TY - JOUR AU - Bateman, G.A. AU - Bateman, A.R. TI - Chronic fatigue syndrome and multiple sclerosis have reduced craniospinal compliance and dilated pressurized bridging cortical veins JF - MEDICAL HYPOTHESES J2 - MED HYPOTHESES VL - 182 PY - 2024 SN - 0306-9877 DO - 10.1016/j.mehy.2023.111243 UR - https://m2.mtmt.hu/api/publication/34525861 ID - 34525861 N1 - Department of Medical Imaging, John Hunter Hospital, Newcastle, NSW, Australia Newcastle University, Faculty of Health, Callaghan Campus, Newcastle, NSW, Australia School of Mechanical Engineering, University of New South Wales, Sydney, NSW, Australia Export Date: 23 January 2024 CODEN: MEHYD Correspondence Address: Bateman, G.A.; Department of Medical Imaging, Locked Bag 1, Newcastle Region Mail Center, 2310, Australia; email: grant.bateman@health.nsw.gov.au AB - Chronic fatigue syndrome (CFS) and multiple sclerosis (MS) share similarities regarding their epidemiology, symptomatology and craniospinal physiology. Indeed, the cardinal feature of CFS, fatigue, is also a major factor in the symptomatology of the majority of MS patients. Recently, we have found that there is a significant reduction in the craniospinal compliance in MS which affects both the stiffness of the walls of the spinal canal and the walls of the cerebral venous system. This change in compliance brings about an alteration in the effectiveness of the pulse wave dampening in the craniospinal system. The result is an impedance mismatch between the cortical veins and their draining sinuses, leading to dilatation of these upstream veins. We deduce this dilatation can only be brought about by an increase in the pressure gradient between the vein lumen and the subarachnoid space (i.e. the transmural pressure gradient). We hypothesise that given the similarities between MS and CFS, a similar mechanism underlies the physiology of CFS. We present two case studies to highlight the expected findings in CFS patients if this hypothesis were proven to be correct. © 2023 LA - English DB - MTMT ER - TY - JOUR AU - Gulej, Rafal AU - Csik, B. AU - Faakye, J. AU - Tarantini, Stefano AU - Shanmugarama, S. AU - Chandragiri, S.S. AU - Mukli, P. AU - Conley, S. AU - Csiszar, Anna AU - Ungvári, Zoltán István AU - Yabluchanskiy, A. AU - Nyúl-Tóth, Ádám TI - Endothelial deficiency of insulin-like growth factor-1 receptor leads to blood–brain barrier disruption and accelerated endothelial senescence in mice, mimicking aspects of the brain aging phenotype JF - MICROCIRCULATION J2 - MICROCIRCULATION VL - 31 PY - 2024 IS - 2 PG - 13 SN - 1073-9688 DO - 10.1111/micc.12840 UR - https://m2.mtmt.hu/api/publication/34444878 ID - 34444878 N1 - Vascular Cognitive Impairment, Neurodegeneration, and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK, United States Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Translational Medicine, Semmelweis University, Budapest, Hungary Export Date: 18 March 2024 CODEN: MROCE Correspondence Address: Yabluchanskiy, A.; Department of Neurosurgery, United States; email: andriy-yabluchanskiy@ouhsc.edu Correspondence Address: Nyúl-Tóth, Á.; Vascular Cognitive Impairment, United States; email: adam-nyultoth@ouhsc.edu Chemicals/CAS: somatomedin C, 67763-96-6; Insulin-Like Growth Factor I; Insulin-Like Peptides LA - English DB - MTMT ER - TY - JOUR AU - Gulej, R. AU - Nyúl-Tóth, Ádám AU - Csik, B. AU - Petersen, B. AU - Faakye, J. AU - Negri, S. AU - Chandragiri, S.S. AU - Mukli, Péter AU - Yabluchanskiy, A. AU - Conley, S. AU - Huffman, D.M. AU - Csiszar, Anna AU - Tarantini, Stefano AU - Ungvári, Zoltán István TI - Rejuvenation of cerebromicrovascular function in aged mice through heterochronic parabiosis: insights into neurovascular coupling and the impact of young blood factors JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 46 PY - 2024 SP - 327 EP - 347 PG - 21 SN - 2509-2715 DO - 10.1007/s11357-023-01039-2 UR - https://m2.mtmt.hu/api/publication/34474845 ID - 34474845 N1 - Vascular Cognitive Impairment, Neurodegeneration, and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Public Health, Semmelweis University, Budapest, Hungary Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK, United States Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, United States Department of Medicine, Albert Einstein College of Medicine, Bronx, NY, United States International Training Program in Geroscience, Doctoral School of Basic and Translational Medicine/Department of Translational Medicine, Semmelweis University, Budapest, Hungary Export Date: 19 March 2024 Correspondence Address: Ungvari, Z.; Vascular Cognitive Impairment, United States; email: zoltan-ungvari@ouhsc.edu Funding details: P20GM125528 Funding details: 101004093/ EUniWell/EAC-A02-2019 / EAC-A02-2019–1 Funding details: 135784, RRF-2.3.1–21-2022–00003 Funding details: P30AG050911 Funding details: U54GM104938 Funding details: National Institute on Aging, NIA, K01AG073613, K01AG073614, R01AG055395, R01AG068295, R01AG070915, R03AG070479, RF1AG072295 Funding details: National Cancer Institute, NCI, P30 CA225520, R01CA255840 Funding details: National Institute of General Medical Sciences, NIGMS Funding details: National Institute of Neurological Disorders and Stroke, NINDS, R01NS100782 Funding details: American Heart Association, AHA, 916225, AHA CDA941290, AHA834339 Funding details: Presbyterian Health Foundation, PHF Funding details: University of Oklahoma Health Sciences Center, OUHSC Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST Funding details: Richard S. Reynolds Foundation Funding details: Oklahoma Tobacco Settlement Endowment Trust, TSET, P30AG038072, TKP2021-NKTA-47 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFI Funding details: Nemzeti Kutatási, Fejlesztési és Innovaciós Alap, NKFIA Funding text 1: We sincerely thank the Division of Comparative Medicine team at the University of Oklahoma Health Sciences Center for their invaluable support in supervising animal care and sharing their extensive expertise. Special recognition is extended to Dr. Shawn Lane, DVM, for his invaluable guidance and expertise in surgical and postsurgical care. We are grateful to Dr. Wendy Williams, DVM, for her instrumental role in designing appropriate pre- and postsurgical treatments. We also acknowledge Ms. Carlye Yancey, BS, for her exceptional animal husbandry knowledge and contributions to parabiosis housing. Furthermore, we wish to express our gratitude to Mr. Chad Cunningham, Electronic & Instrument Shop Supervisor Building Manager of the University of Oklahoma’ s Department of Physics and Engineering for his essential assistance in fabricating the parabiont-adjusted components of the stereotactic frame, which was instrumental in facilitating simultaneous measurements of neurovascular coupling in parabionts. Funding text 2: This work was supported by grants from the American Heart Association (R.G.: 916225, ANT: AHA834339, and S.T.: AHA CDA941290), the Oklahoma Center for the Advancement of Science and Technology, the National Institute on Aging (RF1AG072295, R01AG055395, R01AG068295; R01AG070915, K01AG073614, K01AG073613, R03AG070479), the National Institute of Neurological Disorders and Stroke (R01NS100782), the National Cancer Institute (R01CA255840), the Oklahoma Shared Clinical and Translational Resources (U54GM104938) with an Institutional Development Award (IDeA) from NIGMS, the Presbyterian Health Foundation, the Reynolds Foundation, the Oklahoma Nathan Shock Center (P30AG050911), and the Cellular and Molecular GeroScience CoBRE (P20GM125528), the NCI Cancer Center Support Grant (P30 CA225520) and the Oklahoma Tobacco Settlement Endowment Trust. ANT was supported by Project no. DMH is supported by P30AG038072. TKP2021-NKTA-47, implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-NKTA funding scheme; by funding through the National Cardiovascular Laboratory Program (RRF-2.3.1–21-2022–00003) provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund; Project no. 135784 implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the K_20 funding scheme and the European University for Well-Being (EUniWell) program (grant agreement number: 101004093/ EUniWell/EAC-A02-2019 / EAC-A02-2019–1). The funding sources had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the American Heart Association, or the Presbyterian Health Foundation. The 3.5 version of ChatGPT, developed by OpenAI, was used as a language tool to refine our writing, enhancing the clarity of our work. LA - English DB - MTMT ER - TY - JOUR AU - Miller, L.R. AU - Bickel, M.A. AU - Tarantini, S. AU - Runion, M.E. AU - Matacchiera, Z. AU - Vance, M.L. AU - Hibbs, C. AU - Vaden, H. AU - Nagykaldi, D. AU - Martin, T. AU - Bullen, E.C. AU - Pinckard, J. AU - Kiss, Tamás AU - Howard, E.W. AU - Yabluchanskiy, A. AU - Conley, S.M. TI - IGF1R deficiency in vascular smooth muscle cells impairs myogenic autoregulation and cognition in mice JF - FRONTIERS IN AGING NEUROSCIENCE J2 - FRONT AGING NEUROSCI VL - 16 PY - 2024 PG - 19 SN - 1663-4365 DO - 10.3389/fnagi.2024.1320808 UR - https://m2.mtmt.hu/api/publication/34729965 ID - 34729965 N1 - Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Vascular Cognitive Impairment and Neurodegeneration Program, Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States The Peggy and Charles Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Department of Health Promotion Sciences, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Division of Comparative Medicine, Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States Pediatric Center, Semmelweis University, Budapest, Hungary Eötvös Loránd Research Network and Semmelweis University Cerebrovascular and Neurocognitive Disorders Research Group, Budapest, Hungary Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States Export Date: 5 April 2024 Correspondence Address: Conley, S.M.; Department of Cell Biology, United States; email: Shannon-conley@ouhsc.edu Chemicals/CAS: buprenorphine, 52485-79-7, 53152-21-9 Tradenames: Image Studio version 5.2, LI COR; Odyssey Fc, LI COR; Olympus BX-62, Olympus, United States; QIAcube, Qiagen, United States; RNeasy, Qiagen, United States; thermocycler, Biorad, United States Manufacturers: Biorad, United States; LI COR; Olympus, United States; Qiagen, United States Funding details: T32AG052363 Funding details: P30AG050911 Funding details: U54GM104938 Funding details: National Institutes of Health, NIH, 1P20GM125528, 5P30EY021725-10, 5P30GM122744, K01AG073614, P30CA225520, R01AG070915, R01EY019494, R03AG070479 Funding details: American Heart Association, AHA, AHA941290 Funding details: Presbyterian Health Foundation, PHF Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST Funding details: Oklahoma Center for Adult Stem Cell Research, OCASCR Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Institutes of Health (R01AG070915, R03AG070479, K01AG073614, and R01EY019494) including cores supported as part of (1P20GM125528, 5P30EY021725-10, P30CA225520, and 5P30GM122744), American Heart Association (AHA941290), Hevolution Foundation, Oklahoma Shared Clinical and Translational Resources (U54GM104938), Geroscience Training Program in Oklahoma (T32AG052363), the Oklahoma Nathan Shock Center (P30AG050911), Cellular and Molecular GeroScience CoBRE (1P20GM125528), Presbyterian Health Foundation, Oklahoma Center for Adult Stem Cell Research, and the Oklahoma Center for the Advancement of Science and Technology. Funding agencies had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. LA - English DB - MTMT ER - TY - JOUR AU - Patwardhan, A. AU - Gupta, M. AU - Philip, M. AU - Rangarajan, A. AU - Joshi, T. AU - Alladi, S. AU - Kulkarni, G.B. AU - Ramakrishnan, S. TI - Clinicoradiological Features and Long-term Cognitive and Functional Outcome in Patients with Deep Cerebral Venous Thrombosis JF - ANNALS OF INDIAN ACADEMY OF NEUROLOGY J2 - ANN INDIAN ACAD NEUR VL - 27 PY - 2024 IS - 1 SP - 34 EP - 39 PG - 6 SN - 0972-2327 DO - 10.4103/aian.aian_792_23 UR - https://m2.mtmt.hu/api/publication/34775693 ID - 34775693 N1 - Department of Neurology, National Institute of Mental Health and Neurosciences (NIMHANS), Karnataka, Bengaluru, India Department of Neurology Biostatistics, National Institute of Mental Health and Neurosciences (NIMHANS), Karnataka, Bengaluru, India Export Date: 8 April 2024 Correspondence Address: Ramakrishnan, S.; Department of Neurology, Karnataka, India; email: subasree.ramakrishnan@gmail.com Chemicals/CAS: levetiracetam, 102767-28-2; phenytoin, 57-41-0, 630-93-3 AB - Background: Deep cerebral venous thrombosis (DCVT) can have long-term functional and cognitive sequelae. Although literature exists on cognitive impairment after arterial stroke, cognitive sequelae after cerebral venous thrombosis (CVT) are much less studied. Methods: Clinical records of 29 patients diagnosed with DCVT were reviewed. The Modified Telephonic Interview for Cognitive Status (TICS-M) was adapted and validated in the regional language (Kannada) and applied to 18 patients with DCVT, at a mean follow-up duration of 5.32 years. Screening for depression was done via telephonic Patient Health Questionnaire-9 (PHQ-9)-Kannada version, and functional status was screened by applying the modified Rankin Scale (mRS). Results: DCVT had a mortality rate of 10.34% due to acute complications. mRS scores of 0–1 were achieved at follow-up in all patients who survived. Receiver operating characteristic (ROC) analysis revealed a cutoff of ≤44.5 (maximum score of 49) for the diagnosis of cognitive impairment via TICS-M (Kannada version) in DCVT patients. Evidence of cognitive dysfunction was seen in eight patients (42.10%), and three patients (16.66%) had evidence of depression. Conclusions: Survivors of acute DCVT can potentially have long-term cognitive sequelae. Screening for cognitive dysfunction, depression, and functional status can be effectively done using telephonically applied scales that are adapted to the local language. Neuropsychological evaluation and early cognitive rehabilitation can be initiated for patients in whom deficits are identified on cognitive screening. © 2024 Annals of Indian Academy of Neurology. LA - English DB - MTMT ER - TY - JOUR AU - Tang, C. AU - Zhang, H. AU - Border, J.J. AU - Liu, Y. AU - Fang, X. AU - Jefferson, J.R. AU - Gregory, A. AU - Johnson, C. AU - Lee, T.J. AU - Bai, S. AU - Sharma, A. AU - Shin, S.M. AU - Yu, H. AU - Roman, R.J. AU - Fan, F. TI - Impact of knockout of dual-specificity protein phosphatase 5 on structural and mechanical properties of rat middle cerebral arteries: implications for vascular aging JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - in press PY - 2024 SN - 2509-2715 DO - 10.1007/s11357-024-01061-y UR - https://m2.mtmt.hu/api/publication/34525203 ID - 34525203 N1 - Pharmacology & Toxicology, University of Mississippi Medical Center, Jackson, MS, United States Physiology, Medical College of Georgia, Augusta University, Augusta, GA, United States Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, Augusta, GA, United States Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, United States Export Date: 23 January 2024 Correspondence Address: Fan, F.; Pharmacology & Toxicology, United States; email: ffan@augusta.edu Funding details: National Institutes of Health, NIH Funding details: Augusta University Funding text 1: This study was supported by grants AG079336, AG057842, P20GM104357, and HL138685 from the National Institutes of Health, and TRIBA Faculty Startup Fund from Augusta University. AB - Vascular aging influences hemodynamics, elevating risks for vascular diseases and dementia. We recently demonstrated that knockout (KO) of Dusp5 enhances cerebral and renal hemodynamics and cognitive function. This improvement correlates with elevated pPKC and pERK1/2 levels in the brain and kidneys. Additionally, we observed that Dusp5 KO modulates the passive mechanical properties of cerebral and renal arterioles, associated with increased myogenic tone at low pressure, enhanced distensibility, greater compliance, and reduced stiffness. The present study evaluates the structural and mechanical properties of the middle cerebral artery (MCA) in Dusp5 KO rats. We found that vascular smooth muscle cell layers and the collagen content in the MCA wall are comparable between Dusp5 KO and control rats. The internal elastic lamina in the MCA of Dusp5 KO rats exhibits increased thickness, higher autofluorescence intensity, smaller fenestrae areas, and fewer fenestrations. Despite an enhanced myogenic response and tone of the MCA in Dusp5 KO rats, other passive mechanical properties, such as wall thickness, cross-sectional area, wall-to-lumen ratio, distensibility, incremental elasticity, circumferential wall stress, and elastic modulus, do not significantly differ between strains. These findings suggest that while Dusp5 KO has a limited impact on altering the structural and mechanical properties of MCA, its primary role in ameliorating hemodynamics and cognitive functions is likely attributable to its enzymatic activity on cerebral arterioles. Further research is needed to elucidate the specific enzymatic mechanisms and explore potential clinical applications in the context of vascular aging. © 2024, The Author(s), under exclusive licence to American Aging Association. LA - English DB - MTMT ER - TY - JOUR AU - Wang, J. AU - Manaenko, A. AU - Hu, Q. AU - Zhang, X. TI - Cerebral venous impairment and cerebral venous sinus thrombosis JF - BRAIN HEMORRHAGES J2 - BRAIN HEMORRHAGES VL - in press PY - 2024 SN - 2589-238X DO - 10.1016/j.hest.2024.03.002 UR - https://m2.mtmt.hu/api/publication/34775692 ID - 34775692 N1 - Department of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China Clinical Neuroanatomy Section, Department of Neurology, Ulm University, Ulm, Germany Export Date: 8 April 2024 Correspondence Address: Hu, Q.; Department of Neurosurgery, China; email: huqinle20010709@126.com AB - Cerebral veins are responsible for the outflow drainage of brain interstitial fluid (ISF). The importance of cerebral venous drainage has been emphasized in various neurological diseases. Impaired venous outflow may lead to brain edema, blood–brain barrier (BBB) disruption, inflammatory responses and hemorrhagic complications. With the development of imaging technologies, several imaging-based signs for venous assessment are proposed. Therapies targeting cerebral venous drainage have shown beneficial outcomes in cerebral venous sinus thrombosis (CVST) in clinic, however more insight into the cellular and molecular level should be elucidated. Here we review the pathological changes following cerebral venous drainage impairment, summary the advances in image-based evaluation, address the potential molecular mechanisms, and discuss venous drainage-focused therapies. A better understanding of cerebral venous drainage and its underlying mechanism will promote the pharmacological development and clinical management of CVST. © 2024 International Hemorrhagic Stroke Association LA - English DB - MTMT ER - TY - JOUR AU - Wei, Weipeng AU - Ma, Denglei AU - Li, Lin AU - Zhang, Lan TI - Cognitive impairment in cerebral small vessel disease induced by hypertension JF - NEURAL REGENERATION RESEARCH J2 - NEUR REG RES VL - 19 PY - 2024 IS - 7 SP - 1454 EP - 1462 PG - 9 SN - 1673-5374 DO - 10.4103/1673-5374.385841 UR - https://m2.mtmt.hu/api/publication/34396778 ID - 34396778 N1 - Department of Pharmacy, Xuanwu Hospital of Capital Medical University, Beijing, China Beijing Geriatric Medical Research Center, Beijing Engineering Research Center for Nervous System Drugs, National Center for Neurological Disorders, National Clinical Research Center for Geriatric Diseases, Beijing, China Export Date: 23 January 2024 Correspondence Address: Zhang, L.; Department of Pharmacy, China; email: xwzhanglan@126.com Chemicals/CAS: brain derived neurotrophic factor, 218441-99-7; cyclic AMP responsive element binding protein, 130428-87-4, 130939-96-7 Funding details: ZZ20145 Funding details: DFL20190803 Funding details: Z191100006119017 Funding details: PZ2022006 Funding details: National Natural Science Foundation of China, NSFC, 82104419, 82274611 Funding details: Beijing Municipal Commission of Education, KM202210025017 Funding text 1: Funding: This work was supported by the National Natural Science Foundation of China, Nos. 82274611 (to LZ), 82104419 (to DM); Capital Science and Technology Leading Talent Training Project, No. Z191100006119017 (to LZ); Beijing Hospitals Authority Ascent Plan, No. DFL20190803 (to LZ); Cultivation Fund of Hospital Management Center in Beijing, No. PZ2022006 (to DM); R&D Program of Beijing Municipal Education Commission, No. KM202210025017 (to DM); and Beijing Gold-Bridge Project, No. ZZ20145 (to DM). AB - Hypertension is a primary risk factor for the progression of cognitive impairment caused by cerebral small vessel disease, the most common cerebrovascular disease. However, the causal relationship between hypertension and cerebral small vessel disease remains unclear. Hypertension has substantial negative impacts on brain health and is recognized as a risk factor for cerebrovascular disease. Chronic hypertension and lifestyle factors are associated with risks for stroke and dementia, and cerebral small vessel disease can cause dementia and stroke. Hypertension is the main driver of cerebral small vessel disease, which changes the structure and function of cerebral vessels via various mechanisms and leads to lacunar infarction, leukoaraiosis, white matter lesions, and intracerebral hemorrhage, ultimately resulting in cognitive decline and demonstrating that the brain is the target organ of hypertension. This review updates our understanding of the pathogenesis of hypertension-induced cerebral small vessel disease and the resulting changes in brain structure and function and declines in cognitive ability. We also discuss drugs to treat cerebral small vessel disease and cognitive impairment. LA - English DB - MTMT ER - TY - JOUR AU - Bateman, G.A. AU - Bateman, A.R. AU - Lechner-Scott, J. TI - Dilatation of the bridging cerebral veins in multiple sclerosis correlates with fatigue and suggests an increase in pressure JF - MULTIPLE SCLEROSIS AND RELATED DISORDERS J2 - MULT SCLER RELAT DIS VL - 76 PY - 2023 SN - 2211-0348 DO - 10.1016/j.msard.2023.104843 UR - https://m2.mtmt.hu/api/publication/34055636 ID - 34055636 N1 - Department of Medical Imaging, John Hunter Hospital, Newcastle, NSW, Australia Newcastle University Faculty of Health, Callaghan Campus, Newcastle, NSW, Australia School of Mechanical Engineering, University of New South Wales, Sydney, NSW, Australia Department of Neurology, John Hunter Hospital, Newcastle, NSW, Australia Hunter Medical Research Institute, Newcastle, NSW, Australia Cited By :4 Export Date: 23 January 2024 Correspondence Address: Bateman, G.A.; Department of Medical Imaging, Locked Bag 1, Newcastle Region Mail Center, Australia; email: grant.bateman@health.nsw.gov.au Tradenames: Magnetom Avanto, Siemens, Germany Manufacturers: Siemens, Germany Funding text 1: Not applicable. AB - Background: There is a significant increase in the parenchymal microvessel blood volume in the earliest forms of multiple sclerosis (MS) which may be due to venular dilatation. Increased cortical venous pressure could account for this finding. Venous pressure is also implicated in the physiology of fatigue. The purpose of this study is to discover if there is dilatation of the veins within the subarachnoid space in multiple sclerosis and to estimate the pressures required to maintain any enlargement found. These findings will be correlated with the fatigue symptoms found in MS. Methods: 103 patients with MS were compared with a control group of 50 patients. Post contrast 3DT1 images were used. The cross-sectional area of the bridging cortical veins and the vein of Galen were measured. Results: In MS, the superficial territory cortical veins were 29% larger and the veins of Galen were 25% larger than the controls. Conclusion: There is evidence of a significant increase in the bridging vein transmural pressure in MS, estimated to be approximately 6.5 mmHg in the superficial cortical veins. MS patients with significant fatigue have larger cortical veins than those who are not significantly fatigued. © 2023 LA - English DB - MTMT ER - TY - JOUR AU - da, Silva A.L. AU - Bessa, C.M. AU - Rocha, N.N. AU - Carvalho, E.B. AU - Magalhaes, R.F. AU - Capelozzi, V.L. AU - Robba, C. AU - Pelosi, P. AU - Samary, C.S. AU - Rocco, P.R.M. AU - Silva, P.L. TI - Pressure-support compared with pressure-controlled ventilation mitigates lung and brain injury in experimental acute ischemic stroke in rats JF - INTENSIVE CARE MEDICINE EXPERIMENTAL J2 - INTENSIVE CARE MED EXP VL - 11 PY - 2023 IS - 1 SN - 2197-425X DO - 10.1186/s40635-023-00580-w UR - https://m2.mtmt.hu/api/publication/34525862 ID - 34525862 N1 - Laboratory of Pulmonary Investigation, Centro de Ciências da Saúde, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Avenida Carlos Chagas Filho, S/N, Bloco G-014, Ilha Do Fundão, RJ, Rio de Janeiro, 21941-902, Brazil Department of Physiology and Pharmacology, Biomedical Institute, Fluminense Federal University, Rio de Janeiro, Brazil Department of Pathology, Faculty of Medicine, University of São Paulo, São Paulo, Brazil Department of Surgical Sciences and Integrated Diagnostics (DISC), University of Genoa, Genoa, Italy Anesthesia and Critical Care, San Martino Policlinico Hospital, IRCCS for Oncology and Neurosciences, Genoa, Italy Department of Cardiorespiratory and Musculoskeletal Physiotherapy, Faculty of Physiotherapy, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil Export Date: 23 January 2024 Correspondence Address: Silva, P.L.; Laboratory of Pulmonary Investigation, Avenida Carlos Chagas Filho, S/N, Bloco G-014, Ilha Do Fundão, RJ, Brazil; email: pedroleme@biof.ufrj.br Chemicals/CAS: ketamine, 1867-66-9, 6740-88-1, 81771-21-3; midazolam, 59467-70-8, 59467-96-8; pancuronium bromide, 15500-66-0; protein tyrosine phosphatase; receptor type tyrosine protein phosphatase C; xylazine, 23076-35-9, 7361-61-7 Tradenames: Jelco, Becton Dickinson, United States Manufacturers: Becton Dickinson, United States; National Instruments Funding details: Fundação de Amparo à Pesquisa do Estado de São Paulo, FAPESP, 2018/20493-6 Funding details: Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, CAPES, 88881.371450/2019-01 Funding details: Conselho Nacional de Desenvolvimento Científico e Tecnológico, CNPq, 2019/12151-0 Funding details: Fundação Carlos Chagas Filho de Amparo à Pesquisa do Estado do Rio de Janeiro, FAPERJ, E-26/010.001488/2019, E-26/202.766/2018 Funding text 1: This study was supported by the Brazilian Council for Scientific and Technological Development (CNPq 2019/12151-0), the Rio de Janeiro State Research Foundation (FAPERJ E-26/202.766/2018, E-26/010.001488/2019), the São Paulo State Research Foundation (FAPESP 2018/20493-6), the Coordination for the Improvement of Higher Education Personnel (CAPES 88881.371450/2019-01), and the Department of Science and Technology—Brazilian Ministry of Health (DECIT/MS). Funding text 2: The authors thank Andre Benedito da Silva, BSc, for animal care; Arlete Fernandes, BSc, and Camila Machado, PhD student, for microscopy assistance; Maíra Rezende Lima, MSc, for molecular biology analysis; and Moira Elizabeth Schöttler (Rio de Janeiro, Brazil) and Filippe Vasconcellos (São Paulo, Brazil) for language editing. AB - Background: We aimed to evaluate the pulmonary and cerebral effects of low-tidal volume ventilation in pressure-support (PSV) and pressure-controlled (PCV) modes at two PEEP levels in acute ischemic stroke (AIS). Methods: In this randomized experimental study, AIS was induced by thermocoagulation in 30 healthy male Wistar rats. After 24 h, AIS animals were randomly assigned to PSV or PCV with VT = 6 mL/kg and PEEP = 2 cmH2O (PSV-PEEP2 and PCV-PEEP2) or PEEP = 5 cmH2O (PSV-PEEP5 and PCV-PEEP5) for 2 h. Lung mechanics, arterial blood gases, and echocardiography were evaluated before and after the experiment. Lungs and brain tissue were removed for histologic and molecular biology analysis. The primary endpoint was diffuse alveolar damage (DAD) score; secondary endpoints included brain histology and brain and lung molecular biology markers. Results: In lungs, DAD was lower with PSV-PEEP5 than PCV-PEEP5 (p < 0.001); interleukin (IL)-1β was lower with PSV-PEEP2 than PCV-PEEP2 (p = 0.016) and PSV-PEEP5 than PCV-PEEP5 (p = 0.046); zonula occludens-1 (ZO-1) was lower in PCV-PEEP5 than PCV-PEEP2 (p = 0.042). In brain, necrosis, hemorrhage, neuropil edema, and CD45 + microglia were lower in PSV than PCV animals at PEEP = 2 cmH2O (p = 0.036, p = 0.025, p = 0.018, p = 0.011, respectively) and PEEP = 5 cmH2O (p = 0.003, p = 0.003, p = 0.007, p = 0.003, respectively); IL-1β was lower while ZO-1 was higher in PSV-PEEP2 than PCV-PEEP2 (p = 0.009, p = 0.007, respectively), suggesting blood–brain barrier integrity. Claudin-5 was higher in PSV-PEEP2 than PSV-PEEP5 (p = 0.036). Conclusion: In experimental AIS, PSV compared with PCV reduced lung and brain injury. Lung ZO-1 reduced in PCV with PEEP = 2 versus PEEP = 5 cmH2O, while brain claudin-5 increased in PSV with PEEP = 2 versus PEEP = 5 cmH2O. © 2023, The Author(s). LA - English DB - MTMT ER - TY - JOUR AU - Furon, J. AU - Yetim, M. AU - Pouettre, E. AU - Martinez, de Lizarrondo S. AU - Maubert, E. AU - Hommet, Y. AU - Lebouvier, L. AU - Zheng, Z. AU - Ali, C. AU - Vivien, D. TI - Blood tissue Plasminogen Activator (tPA) of liver origin contributes to neurovascular coupling involving brain endothelial N-Methyl-D-Aspartate (NMDA) receptors JF - FLUIDS AND BARRIERS OF THE CNS J2 - FLUIDS BARRIERS CNS VL - 20 PY - 2023 IS - 1 SN - 2045-8118 DO - 10.1186/s12987-023-00411-w UR - https://m2.mtmt.hu/api/publication/33688898 ID - 33688898 N1 - UNICAEN, INSERM UMR-S U1237, Physiopathology and Imaging of Neurological Disorders (PhIND), GIP Cyceron, Institut Blood and Brain @ Caen-Normandie (BB@C), Normandie University, Bvd Becquerel, BP 5229, Caen, 14074, France Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, United States Blood Research Institute, Versiti Blood Center of Wisconsin, Milwaukee, WI, United States Department of Clinical Research, Caen-Normandie University Hospital, Caen, France Cited By :2 Export Date: 23 January 2024 Correspondence Address: Vivien, D.; UNICAEN, Bvd Becquerel, BP 5229, France; email: vivien@cyceron.fr Chemicals/CAS: tissue plasminogen activator, 105913-11-9; N-Methylaspartate; Receptors, N-Methyl-D-Aspartate; Tissue Plasminogen Activator Funding details: Institut National de la Santé et de la Recherche Médicale, Inserm, EURONANOMED2020-143, U1237-2017/2022 Funding details: Ministère de l'Enseignement Supérieur et de la Recherche, MESR Funding text 1: This work was supported by grants from the Ministère de l’Enseignement Supérieur et de la Recherche and INSERM (French National Institute for Health and Medical Research) (HCERES U1237-2017/2022) and the PLATMED European program (EURONANOMED2020-143). AB - Background: Regulation of cerebral blood flow (CBF) directly influence brain functions and dysfunctions and involves complex mechanisms, including neurovascular coupling (NVC). It was suggested that the serine protease tissue-type plasminogen activator (tPA) could control CNV induced by whisker stimulation in rodents, through its action on N-methyl-d-Aspartate receptors (NMDARs). However, the origin of tPA and the location and mechanism of its action on NMDARs in relation to CNV remained debated. Methods: Here, we answered these issues using tPANull mice, conditional deletions of either endothelial tPA (VECad-CreΔtPA) or endothelial GluN1 subunit of NMDARs (VECad-CreΔGluN1), parabioses between wild-type and tPANull mice, hydrodynamic transfection-induced deletion of liver tPA, hepatectomy and pharmacological approaches. Results: We thus demonstrate that physiological concentrations of vascular tPA, achieved by the bradykinin type 2 receptors-dependent production and release of tPA from liver endothelial cells, promote NVC, through a mechanism dependent on brain endothelial NMDARs. Conclusions: These data highlight a new mechanism of regulation of NVC involving both endothelial tPA and NMDARs. © 2023, The Author(s). LA - English DB - MTMT ER - TY - JOUR AU - Ji, X. TI - Chinese expert consensus on the diagnosis and treatment of venous reflux disorders of head and neck JF - NATIONAL MEDICAL JORNAL OF CHINA/CHINESE MEDICAL JOURNAL J2 - NAT MED J CHINA VL - 103 PY - 2023 IS - 17 SP - 1257 EP - 1279 PG - 23 SN - 0376-2491 DO - 10.3760/cma.j.cn112137-20230112-00069 UR - https://m2.mtmt.hu/api/publication/34399032 ID - 34399032 N1 - Export Date: 23 January 2024 Correspondence Address: Ji, X.; Department of Neurosurgery, China; email: jixm@ccmu.edu.cn Funding details: KM202010025023 Funding details: Z181100001918026 Funding details: National Natural Science Foundation of China, NSFC, 82027802, 82102220, 82271311, T2014251 Funding details: Beijing Municipal Science and Technology Commission, Adminitrative Commission of Zhongguancun Science Park, Z221100007422023 Funding text 1: Cerebral Venous Disease Branch of the Chinese Stroke Association Corresponding author: Ji Xunming, Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China, Email: jixm@ccmu.edu.cn 【Abstract】 Recently, due to the development of medical imaging technology, diseases related to the venous reflux disorders of head and neck have gradually attracted attention. Cerebral Venous Disease Branch of the Chinese Stroke Association developed "Chinese expert consensus on the diagnosis and treatment of venous reflux disorders of head and neck" after repeated discussions covering recent domestic and international advances. The consensus combines the available medical evidence and clinical practice experience, describes three most common types of venous reflux disorders of head and neck, including cerebral venous thrombosis, venous sinus stenosis and internal jugular vein stenosis, systematically summarizes the etiology and risk factors, clinical manifestations, diagnosis and evaluation, treatment and prognosis, and puts forward 71 recommendations, thereby providing the reference for relevant clinicians and researchers. 【Key words】 Cerebrovascular disorders; Venous reflux disorders of head and neck; Cerebral venous diseases; Cerebral venous sinus thrombosis; Intracranial hypertension; Internal jugular venous stenosis; Expert consensus Fund program: National Natural Science Foundation of China (82027802, 82102220, 82271311); Cheung Kong (Chang Jiang) Scholars Program(T2014251); Pharmaceutical Collaboration Project of Beijing Science and Technology Commission (Z181100001918026); Beijing Municipal Science and Technology Commission (Z221100007422023); General Projects of Scientific and Technological Plan of Beijing Municipal Education Commission (KM202010025023) AB - Recently, due to the development of medical imaging technology, diseases related to the venous reflux disorders of head and neck have gradually attracted attention. Cerebral Venous Disease Branch of the Chinese Stroke Association developed "Chinese expert consensus on the diagnosis and treatment of venous reflux disorders of head and neck" after repeated discussions covering recent domestic and international advances. The consensus combines the available medical evidence and clinical practice experience, describes three most common types of venous reflux disorders of head and neck, including cerebral venous thrombosis, venous sinus stenosis and internal jugular vein stenosis, systematically summarizes the etiology and risk factors, clinical manifestations, diagnosis and evaluation, treatment and prognosis, and puts forward 71 recommendations, thereby providing the reference for relevant clinicians and researchers. © 2023 Chinese Medical Association. All rights reserved. LA - Chinese DB - MTMT ER - TY - JOUR AU - Ko, W. AU - Baek, J.-S. AU - Liu, Z. AU - Dong, L. AU - Kim, N. AU - Lee, H. AU - Yoon, C.-S. AU - Kim, N.Y. AU - Kim, S.C. AU - Lee, D.-S. TI - Anti-Inflammatory Activity of 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone Isolated from Cudrania tricuspidata via NF-κB, MAPK, and HO-1 Signaling Pathways in Lipopolysaccharide-Stimulated RAW 264.7 and BV2 Cells JF - MOLECULES J2 - MOLECULES VL - 28 PY - 2023 IS - 21 SN - 1420-3049 DO - 10.3390/molecules28217299 UR - https://m2.mtmt.hu/api/publication/34399031 ID - 34399031 N1 - College of Pharmacy, Wonkwang University, 460, Iksan-daero, Iksan-si, 54538, South Korea Department of Bio-Health Convergence, Kangwon National University, 1, Kangwondaehak-gil, Chuncheon-si, 24341, South Korea College of Pharmacy, Chosun University, 309, Pilmun-daero, Dong-gu, Gwangju, 61452, South Korea Pathology Division, National Institute of Fisheries Science, 216, Gijanghaean-ro, Gijang-eup, Gijang-gun, Busan, 46083, South Korea Department of Family Practice and Community Medicine, Chosun University College of Medicine, 309, Pilmun-daero, Dong-gu, Gwangju, 61452, South Korea Export Date: 23 January 2024 CODEN: MOLEF Correspondence Address: Lee, D.-S.; College of Pharmacy, 309, Pilmun-daero, Dong-gu, South Korea; email: dslee2771@chosun.ac.kr Chemicals/CAS: inducible nitric oxide synthase, 501433-35-8; mitogen activated protein kinase, 142243-02-5; nitric oxide, 10102-43-9; 1,6,7-trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone; Anti-Inflammatory Agents; Cyclooxygenase 2; Interleukin-6; Lipopolysaccharides; Mitogen-Activated Protein Kinases; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II Funding details: Chosun University, CU, K207334004 Funding details: National Institute of Fisheries Science, NIFS, R2023053 Funding text 1: This research was supported by a grant from the National Institute of Fisheries Science (grant number R2023053) and a research fund from Chosun University in 2021 (K207334004). AB - Neuroinflammation activated by microglia affects inflammatory pain development. This study aimed to explore the anti-inflammatory properties and mechanisms of 1,6,7-trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone (THMX) from Cudrania tricuspidata in microglia activation-mediated inflammatory pain. In RAW 264.7 and BV2 cells, THMX has been shown to reduce lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory mediators and cytokines, including nitric oxide (NO), prostaglandin (PG) E2, interleukin (IL)-6, and tumor necrosis factor alpha (TNF-α). THMX also decreased LPS-induced phosphorylation of mitogen-activated protein kinase (MAPK) and the activation of p65 nuclear factor kappa B (NF-κB). Interestingly, THMX also activated heme oxygenase (HO)-1 expression. These findings suggest that THMX is a promising biologically active compound against inflammation through preventing MAPKs and NF-ĸB and activating HO-1 signaling pathways. © 2023 by the authors. LA - English DB - MTMT ER - TY - JOUR AU - Macionis, V. TI - Fetal head-down posture may explain the rapid brain evolution in humans and other primates: An interpretative review JF - BRAIN RESEARCH J2 - BRAIN RES VL - 1820 PY - 2023 SN - 0006-8993 DO - 10.1016/j.brainres.2023.148558 UR - https://m2.mtmt.hu/api/publication/34208621 ID - 34208621 N1 - Export Date: 23 January 2024 CODEN: BRREA Correspondence Address: Macionis, V.Lithuania; email: valdas.macionis.md@gmail.com AB - Evolutionary cerebrovascular consequences of upside-down postural verticality of the anthropoid fetus have been largely overlooked in the literature. This working hypothesis-based report provides a literature interpretation from an aspect that the rapid evolution of the human brain has been promoted by fetal head-down position due to maternal upright and semi-upright posture. Habitual vertical torso posture is a feature not only of humans, but also of monkeys and non-human apes that spend considerable time in a sitting position. Consequently, the head-down position of the fetus may have caused physiological craniovascular hypertension that stimulated expansion of the intracranial vessels and acted as an epigenetic physiological stress, which enhanced neurogenesis and eventually, along with other selective pressures, led to the progressive growth of the anthropoid brain and its organization. This article collaterally opens a new insight into the conundrum of high cephalopelvic proportions (i.e., the tight fit between the pelvic birth canal and fetal head) in phylogenetically distant lineages of monkeys, lesser apes, and humans. Low cephalopelvic proportions in non-human great apes could be accounted for by their energetically efficient horizontal nest-sleeping and consequently by their larger body mass compared to monkeys and lesser apes that sleep upright. One can further hypothesize that brain size varies in anthropoids according to the degree of exposure of the fetus to postural verticality. The supporting evidence for this postulation includes a finding that in fossil hominins cerebral blood flow rate increased faster than brain volume. This testable hypothesis opens a perspective for research on fetal postural cerebral hemodynamics. © 2023 Elsevier B.V. LA - English DB - MTMT ER - TY - JOUR AU - Ni, R.S.S. AU - Mohamed, Raffi H.Q. AU - Dong, Y. TI - The pathophysiology of cognitive impairment in individuals with heart failure: a systematic review JF - FRONTIERS IN CARDIOVASCULAR MEDICINE J2 - FRONT CARDIOVASC MED VL - 10 PY - 2023 SN - 2297-055X DO - 10.3389/fcvm.2023.1181979 UR - https://m2.mtmt.hu/api/publication/34039837 ID - 34039837 N1 - Export Date: 19 January 2024 Correspondence Address: Dong, Y.; Alice Lee Centre for Nursing Studies, Singapore; email: nurdy@nus.edu.sg AB - Introduction: Heart Failure and Cognitive Impairment are both on the rise and shown to be interlinked. Despite existing reviews delineating a relationship between heart failure and cognitive impairment, the underlying pathophysiology is not researched in great depth. Current literature proposed varying pathophysiological mechanisms and focused heavily on the prevalence of cognitive impairment and treatment interventions such as cardiac rehabilitation. In view of the limitations of previous reviews, this systematic review summarized the best existing evidence concerning different pathophysiological mechanisms behind cognitive impairment in individuals with heart failure. Methods: Eight electronic databases including PubMed, Cochrane Library and EMBASE etc., two grey literatures (ProQuest Theses and Dissertations and Mednar) and hand-searching of references were performed using specific criteria regarding population, exposures and outcomes, before duplicate removal and screening using Endnote and Rayyan respectively. JBI critical appraisal tools for non-randomized studies were used for appraisal. Data extraction was performed using two modified forms from JBI Manual for Evidence Synthesis. Results: Narrative synthesis was performed to summarize the data from 32 studies. There were three main themes—cognitive impairment due to changes in the brain: brain atrophy, alterations in grey matter and white matter, cerebral alterations, pathway or axis changes, neuroinflammation and hippocampal gene changes; cognitive impairment due to changes in the heart or systemic circulation: inflammation, oxidative stress and changes in serum biomarkers or proteins and the riser rhythm; cognitive impairment due to changes in both the brain and the heart, with seven studies obtaining negative results. There are some limitations such as having non-human studies and large numbers of cross-sectional studies etc. Discussion: Considering the findings, future research should examine the bi-directional relationship between the brain and the heart as most of the existing research is about the effect of the heart on the brain. By understanding the different pathophysiological mechanisms, the management and prognosis of heart failure patients will be ameliorated. Interventions that slow down or even reverse cognitive impairment can be explored so that these two common issues will not add to the already aggravating disease burden. Systematic Review Registration: This review is registered under PROSPERO. Identifier: CRD42022381359. 2023 Sam, Mohamed Raffi and Dong. LA - English DB - MTMT ER - TY - JOUR AU - Ungvári, Anna Sára AU - Gulej, Rafal AU - Csik, Boglarka AU - Mukli, Péter AU - Negri, Sharon AU - Tarantini, Stefano AU - Yabluchanskiy, Andriy AU - Benyó, Zoltán AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - The Role of Methionine-Rich Diet in Unhealthy Cerebrovascular and Brain Aging: Mechanisms and Implications for Cognitive Impairment JF - NUTRIENTS J2 - NUTRIENTS VL - 15 PY - 2023 IS - 21 PG - 30 SN - 2072-6643 DO - 10.3390/nu15214662 UR - https://m2.mtmt.hu/api/publication/34252131 ID - 34252131 N1 - Department of Public Health, Semmelweis University, Budapest, 1089, Hungary Vascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Oklahoma Center for Geroscience and Healthy Brain Aging, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States International Training Program in Geroscience, Department of Public Health, Doctoral School of Basic and Translational Medicine, Semmelweis University, Budapest, 1089, Hungary Stephenson Cancer Center, University of Oklahoma, Oklahoma City, OK 73104, United States Department of Health Promotion Sciences, College of Public Health, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States Institute of Translational Medicine, Semmelweis University, Budapest, 1094, Hungary Cerebrovascular and Neurocognitive Disorders Research Group, Eötvös Loránd Research Network, Semmelweis University, Budapest, 1094, Hungary International Training Program in Geroscience, Department of Translational Medicine, Doctoral School of Basic and Translational Medicine, Semmelweis University, Budapest, 1089, Hungary Cited By :1 Export Date: 18 January 2024 Correspondence Address: Ungvari, A.; Department of Public Health, Hungary; email: ungann2004@gmail.com Chemicals/CAS: methionine, 59-51-8, 63-68-3, 7005-18-7; Methionine Funding details: P20GM125528 Funding details: 135784, RRF-2.3.1-21-2022-00003 Funding details: P30AG050911 Funding details: U54GM104938 Funding details: National Institutes of Health, NIH Funding details: National Institute on Aging, NIA, K01AG073613, K01AG073614, R01AG055395, R01AG068295, R01AG070915, R03AG070479, RF1AG072295 Funding details: National Cancer Institute, NCI, P30 CA225520, R01CA255840 Funding details: National Institute of General Medical Sciences, NIGMS Funding details: National Institute of Neurological Disorders and Stroke, NINDS, R01NS100782 Funding details: American Heart Association, AHA, AHA 916225, AHA CDA941290 Funding details: Presbyterian Health Foundation, PHF Funding details: Oklahoma Center for the Advancement of Science and Technology, OCAST Funding details: Richard S. Reynolds Foundation Funding details: Oklahoma Tobacco Settlement Endowment Trust, TSET, TKP2021-NKTA-47 Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFI Funding details: Nemzeti Kutatási, Fejlesztési és Innovaciós Alap, NKFIA Funding text 1: This work was supported by grants from the American Heart Association (ST: AHA CDA941290, RG: AHA 916225), the Oklahoma Center for the Advancement of Science and Technology, the National Institute on Aging (RF1AG072295, R01AG055395, R01AG068295; R01AG070915, K01AG073614, K01AG073613, R03AG070479), the National Institute of Neurological Disorders and Stroke (R01NS100782), the National Cancer Institute (R01CA255840), the Oklahoma Shared Clinical and Translational Resources (U54GM104938) with an Institutional Development Award (IDeA) from NIGMS, the Presbyterian Health Foundation, the Reynolds Foundation, the Oklahoma Nathan Shock Center (P30AG050911), and the Cellular and Molecular GeroScience CoBRE (P20GM125528), the NCI Cancer Center Support Grant (P30 CA225520) and the Oklahoma Tobacco Settlement Endowment Trust. AU was supported by Project no. TKP2021-NKTA-47, implemented with the support provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund, financed under the TKP2021-NKTA funding scheme; by funding through the National Cardiovascular Laboratory Program (RRF-2.3.1-21-2022-00003) provided by the Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund; Project no. 135784 implemented with the support provided from the National Research, Development and Innovation Fund of Hungary, financed under the K_20 funding scheme and the European University for Well-Being (EUniWell) program (grant agreement number: 101004093/EUniWell/EAC-A02-2019/EAC-A02-2019-1). The funding sources had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health, the American Heart Association, or the Presbyterian Health Foundation. The 3.5 version of ChatGPT, developed by OpenAI, was used as a language tool to refine our writing, enhancing the clarity of our work. AB - As aging societies in the western world face a growing prevalence of vascular cognitive impairment and Alzheimer’s disease (AD), understanding their underlying causes and associated risk factors becomes increasingly critical. A salient concern in the western dietary context is the high consumption of methionine-rich foods such as red meat. The present review delves into the impact of this methionine-heavy diet and the resultant hyperhomocysteinemia on accelerated cerebrovascular and brain aging, emphasizing their potential roles in cognitive impairment. Through a comprehensive exploration of existing evidence, a link between high methionine intake and hyperhomocysteinemia and oxidative stress, mitochondrial dysfunction, inflammation, and accelerated epigenetic aging is drawn. Moreover, the microvascular determinants of cognitive deterioration, including endothelial dysfunction, reduced cerebral blood flow, microvascular rarefaction, impaired neurovascular coupling, and blood–brain barrier (BBB) disruption, are explored. The mechanisms by which excessive methionine consumption and hyperhomocysteinemia might drive cerebromicrovascular and brain aging processes are elucidated. By presenting an intricate understanding of the relationships among methionine-rich diets, hyperhomocysteinemia, cerebrovascular and brain aging, and cognitive impairment, avenues for future research and potential therapeutic interventions are suggested. LA - English DB - MTMT ER - TY - JOUR AU - Wei, H. AU - Jiang, H. AU - Zhou, Y. AU - Xiao, X. AU - Zhou, C. AU - Ji, X. TI - Cerebral venous congestion alters brain metabolite profiles, impairing cognitive function JF - JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM J2 - J CEREBR BLOOD F MET VL - 43 PY - 2023 IS - 11 SP - 1857 EP - 1872 PG - 16 SN - 0271-678X DO - 10.1177/0271678X231182244 UR - https://m2.mtmt.hu/api/publication/34055638 ID - 34055638 N1 - Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, School of Biological Science and Medical Engineering, Beihang University, Beijing, China Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Beijing Institute of Brain Disorders, Beijing Advanced Innovation Center for Big Data-based Precision Medicine, Capital Medical University, Beijing, China Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing, China Export Date: 19 January 2024 CODEN: JCBMD Correspondence Address: Ji, X.; Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, China; email: chenzhou2013abc@163.com Correspondence Address: Zhou, C.; Laboratory of Brain Disorders, China; email: jixm@ccmu.edu.cn Chemicals/CAS: 4 aminobutyric acid, 28805-76-7, 56-12-2; acetylcysteine, 616-91-1; alanine, 56-41-7, 6898-94-8; aspartic acid, 56-84-8, 6899-03-2; butyric acid, 107-92-6, 156-54-7, 461-55-2; isoleucine, 7004-09-3, 73-32-5; leucine, 61-90-5, 7005-03-0; methionine, 59-51-8, 63-68-3, 7005-18-7; nicotinamide, 11032-50-1, 98-92-0; nicotinic acid, 54-86-4, 59-67-6; threonine, 36676-50-3, 72-19-5; tyrosine, 16870-43-2, 55520-40-6, 60-18-4; valine, 7004-03-7, 72-18-4 Manufacturers: RWD, ChinaBiovision; Cloud-Clone; RWD, China; Thermo, United States; Waters, United States Funding details: Z181100001918026 Funding details: National Natural Science Foundation of China, NSFC, 82271311 Funding text 1: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Cheung Kong (Changjiang) Scholars Program (T2014251), the Pharmaceutical Collaboration Project of Beijing Science and Technology Commission (Z181100001918026), grants from National Natural Science Foundation of China (82271311). AB - Vascular cognitive impairment (VCI) represents the second most common cause of dementia after Alzheimer's disease, and pathological changes in cerebral vascular structure and function are pivotal causes of VCI. Cognitive impairment caused by arterial ischemia has been extensively studied the whole time; the influence of cerebral venous congestion on cognitive impairment draws doctors’ attention in recent clinical practice, but the underlying neuropathophysiological alterations are not completely understood. This study elucidated the specific pathogenetic role of cerebral venous congestion in cognitive-behavioral deterioration and possible electrophysiological mechanisms. Using cerebral venous congestion rat models, we found these rats exhibited decreased long-term potentiation (LTP) in the hippocampal dentate gyrus and impaired spatial learning and memory. Based on untargeted metabolomics, N-acetyl-L-cysteine (NAC) deficiency was detected in cerebral venous congestion rats; supplementation with NAC appeared to ameliorate synaptic deficits, rescue impaired LTP, and mitigate cognitive impairment. In a cohort of cerebral venous congestion patients, NAC levels were decreased; NAC concentration was negatively correlated with subjective cognitive decline (SCD) score but positively correlated with mini-mental state examination (MMSE) score. These findings provide a new perspective on cognitive impairment and support further exploration of NAC as a therapeutic target for the prevention and treatment of VCI. © The Author(s) 2023. LA - English DB - MTMT ER - TY - JOUR AU - Wu, Y. AU - Chen, L. AU - Zhong, F. AU - Zhou, K. AU - Lu, C. AU - Cheng, X. AU - Wang, S. TI - Cognitive impairment in patients with heart failure: molecular mechanism and therapy JF - HEART FAILURE REVIEWS J2 - HEART FAIL REV VL - 28 PY - 2023 IS - 4 SP - 807 EP - 820 PG - 14 SN - 1382-4147 DO - 10.1007/s10741-022-10289-9 UR - https://m2.mtmt.hu/api/publication/33551588 ID - 33551588 N1 - Department of Anesthesiology, School of Medicine, South China University of Technology, Guangzhou, 510006, China Department of Anesthesiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China Department of Anesthesiology, Guangdong Province, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China Department of Anesthesiology, The First Affiliated Hospital of Jinan University, Guangdong, Guangzhou, 510630, China Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China Cited By :1 Export Date: 21 December 2023 CODEN: HFREF Correspondence Address: Wang, S.; Department of Anesthesiology, China; email: shengwang_gz@163.com Chemicals/CAS: cystic fibrosis transmembrane conductance regulator, 126880-72-6; talfirastide, 39386-80-6, 51833-78-4 AB - Heart failure (HF) is associated with multiple organ dysfunction and many comorbidities. Its incidence is high among the elderly and is a major health burden worldwide. Cognitive impairment (CI) is highly prevalent in older patients with HF, which is an abnormality in one or more of the items of cognition, attention, memory, language, psychomotor function, and visual spatial acuity. Studies have shown that the incidence of CI in HF patients is between 13 and 54%, and patients with both conditions have poor self-care ability and prognosis, as well as increased mortality rates. However, the mechanisms of CI development in HF patients are still unclear. In this review, we describe the epidemiology and risk factors as well as measures of improving CI in HF patients. We update the latest pathophysiological mechanisms related to the neurocognitive changes in HF patients, expounding on the mechanisms associated with the development of CI in HF patients. © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. LA - English DB - MTMT ER - TY - JOUR AU - Bateman, A.R. AU - Lechner-Scott, J. AU - Barber, T. AU - Bateman, G.A. AU - Ramadan, S. TI - Quantified hemodynamic parameters of the venous system in multiple sclerosis: A systematic review JF - MULTIPLE SCLEROSIS AND RELATED DISORDERS J2 - MULT SCLER RELAT DIS VL - 57 PY - 2022 SN - 2211-0348 DO - 10.1016/j.msard.2021.103477 UR - https://m2.mtmt.hu/api/publication/32682118 ID - 32682118 AB - Background: Multiple Sclerosis (MS) is a complex neurodegenerative condition that is influenced by a combination of genetic and environmental factors. Included in these factors is the venous system, however, the extent to which it influences the etiology of MS has yet to be fully characterised. The aim of this review is to critically summarize the literature available concerning the venous system in MS, primarily concerning specific data on the venous pressure and blood flow in this system. Methods: A systematic review was conducted with the application of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. The advanced search functions of both the Scopus and PubMed databases were used to conduct the literature search, resulting in 136 unique articles initially identified. Applying relevant exclusion criteria, 22 of the studies were chosen for this review. Results: The selected studies were analysed for venous pressure and blood flow related findings, with 14 studies contributing data on the internal jugular vein (IJV) flow rate, 5 on blood flows of the intracranial venous sinuses, 2 on blood flow pulsatility and 6 supplying information relevant to the venous pressure (3 studies contributed to multiple areas). The general findings of the review included that the IJV flow was not significantly different between MS patients and controls, however, there were variances between stenotic (S) and non-stenotic (NS) MS patients. Due to the limited data in the other two areas defined in this review, further research is required to establish if any variances in MS are present. Conclusion: It remains unclear if there are significant differences in many flow variables between MS patients and controls considered in this review. It would be advantageous if future work in this area focused on understanding the hemodynamics of this system, primarily concerning how the flow rate, venous pressure and vascular resistance are related, and any impact that these factors have on the etiology of MS. © 2021 Elsevier B.V. LA - English DB - MTMT ER - TY - JOUR AU - Cao, T.Q. AU - Liu, Z. AU - Dong, L. AU - Lee, H. AU - Ko, W. AU - Vinh, L.B. AU - Tuan, N.Q. AU - Kim, Y.-C. AU - Sohn, J.H. AU - Yim, J.H. AU - Lee, D.-S. AU - Oh, H. TI - Identification of Potential Anti‐Neuroinflammatory Inhibitors from Antarctic Fungal Strain Aspergillus sp. SF‐7402 via Regulating the NF‐κB Signaling Pathway in Microglia JF - MOLECULES J2 - MOLECULES VL - 27 PY - 2022 IS - 9 SN - 1420-3049 DO - 10.3390/molecules27092851 UR - https://m2.mtmt.hu/api/publication/32870866 ID - 32870866 AB - Microglia play a significant role in immune defense and tissue repair in the central nervous system (CNS). Microglial activation and the resulting neuroinflammation play a key role in the pathogenesis of neurodegenerative disorders. Recently, inflammation reduction strategies in neurodegenerative diseases have attracted increasing attention. Herein, we discovered and evaluated the anti‐neuroinflammatory potential of compounds from the Antarctic fungi strain Aspergil-lus sp. SF‐7402 in lipopolysaccharide (LPS)‐stimulated BV2 cells. Four metabolites were isolated from the fungi through chemical investigations, namely, 5‐methoxysterigmatocystin (1), sterig-matocystin (2), aversin (3), and 6,8‐O‐dimethylversicolorin A (4). Their chemical structures were elucidated by extensive spectroscopic analysis and HR‐ESI‐MS, as well as by comparison with those reported in literature. Anti‐neuroinflammatory effects of the isolated metabolites were evaluated by measuring the production of nitric oxide (NO), tumor necrosis factor (TNF)‐α, and interleukin (IL)‐6 in LPS‐activated microglia at non‐cytotoxic concentrations. Sterigmatocystins (1 and 2) displayed significant effects on NO production and mild effects on TNF‐α and IL‐6 expression inhibition. The molecular mechanisms underlying this activity were investigated using Western blot analysis. Sterigmatocystin treatment inhibited NO production via downregulation of inducible nitric oxide synthase (iNOS) expression in LPS‐stimulated BV2 cells. Additionally, ster-igmatocystins reduced nuclear translocation of NF‐κB. These results suggest that sterigmatocystins present in the fungal strain Aspergillus sp. are promising candidates for the treatment of neuroin-flammatory diseases. © 2022 by the authors. Licensee MDPI, Basel, Switzerland. LA - English DB - MTMT ER - TY - JOUR AU - Nyúl-Tóth, Ádám AU - Fülöp, Gábor Áron AU - Tarantini, Stefano AU - Kiss, Tamás AU - Ahire, Chetan AU - Faakye, Janet A AU - Ungvári, Anna Sára AU - Tóth, Péter József AU - Tóth, Attila AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Cerebral venous congestion exacerbates cerebral microhemorrhages in mice JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 44 PY - 2022 SP - 805 EP - 816 PG - 12 SN - 2509-2715 DO - 10.1007/s11357-021-00504-0 UR - https://m2.mtmt.hu/api/publication/32590647 ID - 32590647 AB - Cerebral microhemorrhages (CMHs; microbleeds), which are small focal intracerebral hemorrhages, importantly contribute to the pathogenesis of cognitive decline and dementia in older adults. Although recently it has been increasingly recognized that the venous side of the cerebral circulation likely plays a fundamental role in the pathogenesis of a wide spectrum of cerebrovascular and brain disorders, its role in the pathogenesis of CMHs has never been studied. The present study was designed to experimentally test the hypothesis that venous congestion can exacerbate the genesis of CMHs. Increased cerebral venous pressure was induced by internal and external jugular vein ligation (JVL) in C57BL/6 mice in which systemic hypertension was induced by treatment with angiotensin II plus L-NAME. Histological analysis (diaminobenzidine staining) showed that mice with JVL developed multiple CMHs. CMHs in mice with JVL were often localized adjacent to veins and venules and their morphology was consistent with venous origin of the bleeds. In brains of mice with JVL, a higher total count of CMHs was observed compared to control mice. CMHs were distributed widely in the brain of mice with JVL, including the cortical gray matter, brain stem, the basal ganglia, subcortical white matter, cerebellum, and the hippocampi. In mice with JVL, there were more CMHs predominantly in cerebral cortex, brain stem, and cerebellum than in control mice. CMH burden, defined as total CMH volume, also significantly increased in mice with JVL. Thus, cerebral venous congestion can exacerbate CMHs. These observations have relevance to the pathogenesis of cognitive impairment associated with right heart failure as well as elevated cerebral venous pressure due to jugular venous reflux in older adults. LA - English DB - MTMT ER - TY - JOUR AU - Primiani, C.T. AU - Lawton, M. AU - Hillis, A.E. AU - Hui, F.K. TI - Pearls & Oy-sters: Cerebral Venous Congestion Associated With Cognitive Decline Treated by Jugular Release JF - NEUROLOGY J2 - NEUROLOGY VL - 99 PY - 2022 IS - 13 SP - 577 EP - 580 PG - 4 SN - 0028-3878 DO - 10.1212/WNL.0000000000201037 UR - https://m2.mtmt.hu/api/publication/33185900 ID - 33185900 AB - Cognitive dysfunction is often multifaceted and can be seen across all age groups in medicine. The combination of cognitive decline and increased intracranial pressure may suggest possible anatomical abnormalities. We present a case report from our academic center that describes a young man with new cognitive fatigue and brain fog in the setting of increased venous pressure that resolved with surgical intervention at a site of jugular vein stenosis. We discuss current hypotheses from basic and clinical research related to pathophysiology underlying venous vascular congestion and associated neurologic disorders. Further research is warranted to elucidate the underlying mechanisms of venous congestion and cognition to better identify therapies and improve quality of life for patients. © American Academy of Neurology. LA - English DB - MTMT ER - TY - CHAP AU - Qu, B. AU - Rui, Z. ED - Sun, H. TI - Study on blood vessel segmentation of laser scattering microscopic image T2 - 4th IEEE International Conference on Civil Aviation Safety and Information Technology, ICCASIT 2022 PB - Institute of Electrical and Electronics Engineers (IEEE) CY - Piscataway (NJ) SN - 1665467665 PY - 2022 SP - 1294 EP - 1299 PG - 6 DO - 10.1109/ICCASIT55263.2022.9986646 UR - https://m2.mtmt.hu/api/publication/33599620 ID - 33599620 AB - Laser scatter imaging (LSCI) is a powerful method for analyzing blood flow in the human vasculature. Due to its advantages of non-contact, non-invasive and fast imaging, laser scattering imaging is increasingly being used in fundus vascular imaging. The research in this paper will contribute to the vascular segmentation of laser scattering microscopic images and their quantitative analysis. In this paper, the vascular segmentation algorithms for fundus scattered vascular images are investigated separately, and the segmentation effects of traditional and U-Net-based deep learning algorithms are compared. Based on the U-Net network, we propose a Recurrent-U-Net structure based on circular convolution and compare it with other algorithms. The results show that the deep learning segmentation algorithm outperforms traditional algorithms. Moreover, the Recurrent-U-Net network can reduce the problem of losing tiny vessels in the U-Net network and further improve the segmentation effect. © 2022 IEEE. LA - English DB - MTMT ER - TY - JOUR AU - Yijing, J. AU - Cancan, L. AU - Yuanxiao, W. AU - Liqun, F. TI - Study on relationship between venous system and white matter hyperintensitiy in cerebral small vessel disease JF - CLINICAL MEDICINE OF CHINA J2 - CLINICAL MEDICINE OF CHINA VL - 38 PY - 2022 IS - 3 SP - 284 EP - 288 PG - 5 SN - 1008-6315 DO - 10.3760/cma.j.cn101721-20211021-000192 UR - https://m2.mtmt.hu/api/publication/33025364 ID - 33025364 AB - White matter hyperintensity (WMH) is one of the major imaging markers of cerebral small vascular disease, which is prevalent in the elderly. At present, the pathogenesis of WMH is not clear, most of the previous studies focused on the arterial system, but the role of the venous system in WMH is attracting more and more attention. Small venous collagen hyperplasia, downstream intracranial venous dilatation and internal jugular venous reflux may be involved in the formation and development of white matter hyperintensity. © 2022, Chinese Medical Journals Publishing House Co.Ltd. All rights reserved. LA - Chinese DB - MTMT ER - TY - JOUR AU - Balasubramanian, Priya AU - Kiss, Tamás AU - Tarantini, Stefano AU - Nyúl-Tóth, Ádám AU - Ahire, Chetan AU - Yabluchanskiy, Andriy AU - Csípő, Tamás AU - Lipécz, Ágnes AU - Tabák, Ádám AU - Institoris, Adam AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Obesity-induced cognitive impairment in older adults: a microvascular perspective JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 320 PY - 2021 IS - 2 SP - H740 EP - H761 PG - 22 SN - 0363-6135 DO - 10.1152/ajpheart.00736.2020 UR - https://m2.mtmt.hu/api/publication/31923447 ID - 31923447 N1 - Funding Agency and Grant Number: Oklahoma Center for the Advancement of Science and Technology; National Institute on Aging (NIA) [R01-AG047879, R01-AG038747, R01-AG055395, R01-AG068295]; National Institute of Neurological Disorders and Stroke [R01-NS056218, R01-NS100782]; National Institute of General Medical Sciences Oklahoma Shared Clinical and Translational Resources [GM104938]; Presbyterian Health Foundation; Oklahoma Nathan Shock Center [P30AG050911]; Cellular and Molecular GeroScience CoBRE [1P20GM125528, 5337]; NIA [T32AG052363] Funding text: This work was supported by grants from the Oklahoma Center for the Advancement of Science and Technology (to A. Csiszar, A. Yabluchanskiy, and Z. Ungvari), the National Institute on Aging (NIA; R01-AG047879; R01-AG038747; R01-AG055395; R01-AG068295), the National Institute of Neurological Disorders and Stroke (R01-NS056218, R01-NS100782), the National Institute of General Medical Sciences Oklahoma Shared Clinical and Translational Resources (GM104938, to A. Yabluchanskiy), the Presbyterian Health Foundation, the NIA-supported Geroscience Training Program in Oklahoma (T32AG052363), the Oklahoma Nathan Shock Center (P30AG050911), the Cellular and Molecular GeroScience CoBRE (1P20GM125528, sub#5337). AB - Over two-thirds of individuals aged 65 and older are obese or overweight in the United States. Epidemiological data show an association between the degree of adiposity and cognitive dysfunction in the elderly. In this review, the pathophysiological roles of microvascular mechanisms, including impaired endothelial function and neurovascular coupling responses, microvascular rarefaction, and blood-brain barrier disruption in the genesis of cognitive impairment in geriatric obesity are considered. The potential contribution of adipose-derived factors and fundamental cellular and molecular mechanisms of senescence to exacerbated obesity-induced cerebromicrovascular impairment and cognitive decline in aging are discussed. LA - English DB - MTMT ER - TY - JOUR AU - Dayer, Mark AU - MacIver, David H. AU - Rosen, Stuart D. TI - The central nervous system and heart failure JF - FUTURE CARDIOLOGY J2 - FUTURE CARDIOL VL - 17 PY - 2021 IS - 2 SP - 363 EP - 382 PG - 20 SN - 1479-6678 DO - 10.2217/fca-2020-0059 UR - https://m2.mtmt.hu/api/publication/31624021 ID - 31624021 N1 - Department of Cardiology, Musgrove Park Hospital, Taunton, TA1 5DA, United Kingdom Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, M13 9PL, United Kingdom Ealing and Royal Brompton Hospitals, Uxbridge Rd, Southall, UB1 3HW, United Kingdom Imperial College London, South Kensington, London, SW7 2BU, United Kingdom Cited By :1 Export Date: 11 January 2024 Correspondence Address: Dayer, M.; Department of Cardiology, United Kingdom; email: markdayer@me.com AB - The view that chronic heart failure was exclusively a disease of the heart dominated the cardiovascular literature until relatively recently. However, over the last 40 years it has increasingly come to be seen as a multisystem disease. Aside from changes in the sympathetic and parasympathetic nervous systems and the renin-angiotensin-aldosterone system, adaptations to the lungs, muscles and gastrointestinal tract have been clearly documented. It is clear that the brain and CNS are also affected in patients with heart failure, although this is often under recognized. The purpose of this review is to summarize the changes in the structure and biochemical function of the CNS in patients with chronic heart failure and to discuss their potential importance. LA - English DB - MTMT ER - TY - JOUR AU - Kapadia, A. AU - Dmytriw, A.A. TI - Venous dysfunction plays a critical role in “normal” white matter disease of aging JF - MEDICAL HYPOTHESES J2 - MED HYPOTHESES VL - 146 PY - 2021 SN - 0306-9877 DO - 10.1016/j.mehy.2020.110457 UR - https://m2.mtmt.hu/api/publication/31836015 ID - 31836015 LA - English DB - MTMT ER - TY - JOUR AU - Liu, Y. AU - Zhang, H. AU - Wang, S. AU - Guo, Y. AU - Fang, X. AU - Zheng, B. AU - Gao, W. AU - Yu, H. AU - Chen, Z. AU - Roman, R.J. AU - Fan, F. TI - Reduced pericyte and tight junction coverage in old diabetic rats are associated with hyperglycemia-induced cerebrovascular pericyte dysfunction JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 320 PY - 2021 IS - 2 SP - H549 EP - H562 SN - 0363-6135 DO - 10.1152/AJPHEART.00726.2020 UR - https://m2.mtmt.hu/api/publication/31907081 ID - 31907081 AB - Diabetes mellitus (DM) is one of the primary pathological factors that contributes to aging-related cognitive impairments, but the underlying mechanisms remain unclear. We recently reported that old DM rats exhibited impaired myogenic responses of the cerebral arteries and arterioles, poor cerebral blood flow autoregulation, enhanced blood-brain barrier (BBB) leakage, and cognitive impairments. These changes were associated with diminished vascular smooth muscle cell contractile capability linked to elevated reactive oxygen species (ROS) and reduced ATP production. In the present study, using a nonobese T2DN DM rat, we isolated parenchymal arterioles (PAs), cultured cerebral microvascular pericytes, and examined whether cerebrovascular pericyte in DM is damaged and whether pericyte dysfunction may play a role in the regulation of cerebral hemodynamics and BBB integrity. We found that ROS and mitochondrial superoxide production were elevated in PAs isolated from old DM rats and in high glucose (HG)-treated a-smooth muscle actin-positive pericytes. HG-treated pericytes displayed decreased contractile capability in association with diminished mitochondrial respiration and ATP production. Additionally, the expression of advanced glycation end products, transforming growth factor-b, vascular endothelial growth factor, and fibronectin were enhanced, but claudin 5 and integrin b1 was reduced in the brain of old DM rats and HG-treated pericytes. Further, endothelial tight junction and pericyte coverage on microvessels were reduced in the cortex of old DM rats. These results demonstrate our previous findings that the impaired cerebral hemodynamics and BBB leakage and cognitive impairments in the same old DM model are associated with hyperglycemia-induced cerebrovascular pericyte dysfunction. NEW & NOTEWORTHY This study demonstrates that the loss of contractile capability in pericytes in diabetes is associated with enhanced ROS and reduced ATP production. Enhanced advanced glycation end products (AGEs) in diabetes accompany with reduced pericyte and endothelial tight junction coverage in the cortical capillaries of old diabetic rats. These results suggest our previous findings that the impaired cerebral hemodynamics, BBB leakage, and cognitive impairments in old DM model are associated with hyperglycemia-induced cerebrovascular pericyte dysfunction. Copyright © 2021 the American Physiological Society LA - English DB - MTMT ER - TY - JOUR AU - Luo, A. AU - Li, S. AU - Wang, X. AU - Xie, Z. AU - Li, S. AU - Hua, D. TI - Cefazolin Improves Anesthesia and Surgery-Induced Cognitive Impairments by Modulating Blood-Brain Barrier Function, Gut Bacteria and Short Chain Fatty Acids JF - FRONTIERS IN AGING NEUROSCIENCE J2 - FRONT AGING NEUROSCI VL - 13 PY - 2021 SN - 1663-4365 DO - 10.3389/fnagi.2021.748637 UR - https://m2.mtmt.hu/api/publication/32558712 ID - 32558712 AB - Emerging evidence suggests that anesthesia and surgery may induce gut dysbiosis. Gut dysbiosis leads to imbalance in circulating contents of microbiota-derived metabolites and disrupts the integrity of the blood-brain barrier (BBB), contributing to postoperative cognitive dysfunction (POCD). The composition of gut microbiota may be influenced by various antibiotics. However, how perioperative use of antibiotics affects POCD needs more explorations. In the present study, we explored the effect of cefazolin, a common antibiotic used in perioperative period, on cognitive function, BBB integrity, gut bacteria and short chain fatty acids (SCFAs), a group of widely studied metabolites in aged mice, using 18-month-old male mice. Significant BBB disruptions and decreased levels of tight junction proteins, zonula occludens-1 (ZO-1) and Occludin (OCLN) were seen in the mice of POCD model. Cefazolin treatment attenuated these changes induced by anesthesia and surgery. Furthermore, cefazolin reversed the changes in several fecal bacteria (β-, γ/δ-, ε-Proteobacteria, and Bacteroidetes) as determined by qPCR tests. Analysis of plasma SCFAs showed that almost all types of SCFAs were reduced in POCD and cefazolin administration reversed the changes in expression of the two most abundant SCFAs (acetic and propionic acids). In conclusion, this study demonstrated that cefazolin improved POCD. Mechanistically, cefazolin suppressed the disruption of BBB, gut microbiota or SCFAs, thereby ameliorating POCD. © Copyright © 2021 Luo, Li, Wang, Xie, Li and Hua. LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Andrea Ágnes AU - Nádasy, György László AU - Bednárikné Dörnyei, Gabriella AU - Patai, Bernadett Bettina AU - Delfavero, J. AU - Fülöp, Gábor Áron AU - Kirkpatrick, A.C. AU - Ungvári, Zoltán István AU - Merkely, Béla Péter TI - The aging venous system: from varicosities to vascular cognitive impairment JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 43 PY - 2021 IS - 6 SP - 2761 EP - 2784 PG - 24 SN - 2509-2715 DO - 10.1007/s11357-021-00475-2 UR - https://m2.mtmt.hu/api/publication/32505562 ID - 32505562 N1 - Export Date: 3 April 2024 AB - Aging-induced pathological alterations of the circulatory system play a critical role in morbidity and mortality of older adults. While the importance of cellular and molecular mechanisms of arterial aging for increased cardiovascular risk in older adults is increasingly appreciated, aging processes of veins are much less studied and understood than those of arteries. In this review, age-related cellular and morphological alterations in the venous system are presented. Similarities and dissimilarities between arterial and venous aging are highlighted, and shared molecular mechanisms of arterial and venous aging are considered. The pathogenesis of venous diseases affecting older adults, including varicose veins, chronic venous insufficiency, and deep vein thrombosis, is discussed, and the potential contribution of venous pathologies to the onset of vascular cognitive impairment and neurodegenerative diseases is emphasized. It is our hope that a greater appreciation of the cellular and molecular processes of vascular aging will stimulate further investigation into strategies aimed at preventing or retarding age-related venous pathologies. © 2021, The Author(s). LA - English DB - MTMT ER - TY - JOUR AU - Molnár, Tihamér AU - Ezer, Erzsébet TI - Neurointenzív Tanszék – az első év JF - FOCUS MEDICINAE J2 - FOCUS MEDICINAE VL - 23 PY - 2021 IS - 1 SP - 3 EP - 5 PG - 3 SN - 1419-0478 UR - https://m2.mtmt.hu/api/publication/31963966 ID - 31963966 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Nyúl-Tóth, Ádám AU - Tarantini, Stefano AU - DelFavero, J. AU - Yan, F. AU - Balasubramanian, P. AU - Yabluchanskiy, A. AU - Ahire, C. AU - Kiss, Tamás AU - Csípő, Tamás AU - Lipécz, Ágnes AU - Farkas, Elek Attila AU - Wilhelm, Imola Mária AU - Krizbai, István Adorján AU - Tang, Q. AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Demonstration of age-related blood-brain barrier disruption and cerebromicrovascular rarefaction in mice by longitudinal intravital two-photon microscopy and optical coherence tomography JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 320 PY - 2021 IS - 4 SP - H1370 EP - H1392 PG - 23 SN - 0363-6135 DO - 10.1152/ajpheart.00709.2020 UR - https://m2.mtmt.hu/api/publication/31967308 ID - 31967308 AB - Age-related blood-brain barrier (BBB) disruption and cerebromicrovascular rarefaction contribute importantly to the pathogenesis of both vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). Recent advances in geroscience research enable development of novel interventions to reverse age-related alterations of the cerebral microcirculation for prevention of VCID and AD. To facilitate this research, there is an urgent need for sensitive and easy-to-adapt imaging methods that enable longitudinal assessment of changes in BBB permeability and brain capillarization in aged mice and that could be used in vivo to evaluate treatment efficiency. To enable longitudinal assessment of changes in BBB permeability in aged mice equipped with a chronic cranial window, we adapted and optimized two different intravital two-photon imaging approaches. By assessing relative fluorescence changes over the baseline within a volume of brain tissue, after qualitative image subtraction of the brain microvasculature, we confirmed that, in 24-mo-old C57BL/6J mice, cumulative permeability of the microvessels to fluorescent tracers of different molecular masses (0.3 to 40 kDa) is significantly increased compared with that of 5-mo-old mice. Real-time recording of vessel cross-sections showed that apparent solute permeability of single microvessels is significantly increased in aged mice vs. young mice. Cortical capillary density, assessed both by intravital two-photon microscopy and optical coherence tomography was also decreased in aged mice vs. young mice. The presented methods have been optimized for longitudinal (over the period of 36 wk) in vivo assessment of cerebromicrovascular health in preclinical geroscience research.NEW & NOTEWORTHY Methods are presented for longitudinal detection of age-related increase in blood-brain barrier permeability and microvascular rarefaction in the mouse cerebral cortex by intravital two-photon microscopy and optical coherence tomography. LA - English DB - MTMT ER - TY - JOUR AU - Ungvári, Zoltán István AU - Tóth, Péter József AU - Tarantini, Stefano AU - Prodan, Calin I AU - Sorond, Farzaneh AU - Merkely, Béla Péter AU - Csiszar, Anna TI - Hypertension-induced cognitive impairment : from pathophysiology to public health JF - NATURE REVIEWS NEPHROLOGY J2 - NAT REV NEPHROL VL - 17 PY - 2021 IS - 10 SP - 639 EP - 654 PG - 16 SN - 1759-5061 DO - 10.1038/s41581-021-00430-6 UR - https://m2.mtmt.hu/api/publication/32074149 ID - 32074149 AB - Hypertension affects two-thirds of people aged >60 years and significantly increases the risk of both vascular cognitive impairment and Alzheimer's disease. Hypertension compromises the structural and functional integrity of the cerebral microcirculation, promoting microvascular rarefaction, cerebromicrovascular endothelial dysfunction and neurovascular uncoupling, which impair cerebral blood supply. In addition, hypertension disrupts the blood-brain barrier, promoting neuroinflammation and exacerbation of amyloid pathologies. Ageing is characterized by multifaceted homeostatic dysfunction and impaired cellular stress resilience, which exacerbate the deleterious cerebromicrovascular effects of hypertension. Neuroradiological markers of hypertension-induced cerebral small vessel disease include white matter hyperintensities, lacunar infarcts and microhaemorrhages, all of which are associated with cognitive decline. Use of pharmaceutical and lifestyle interventions that reduce blood pressure, in combination with treatments that promote microvascular health, have the potential to prevent or delay the pathogenesis of vascular cognitive impairment and Alzheimer's disease in patients with hypertension. LA - English DB - MTMT ER - TY - JOUR AU - Ventoulis, I. AU - Arfaras-Melainis, A. AU - Parissis, J. AU - Polyzogopoulou, E. TI - Cognitive impairment in acute heart failure: Narrative review JF - JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE J2 - J CARDIOVASC DEV DIS VL - 8 PY - 2021 IS - 12 SN - 2308-3425 DO - 10.3390/jcdd8120184 UR - https://m2.mtmt.hu/api/publication/32558711 ID - 32558711 AB - Cognitive impairment (CI) represents a common but often veiled comorbidity in patients with acute heart failure (AHF) that deserves more clinical attention. In the AHF setting, it manifests as varying degrees of deficits in one or more cognitive domains across a wide spectrum ranging from mild CI to severe global neurocognitive disorder. On the basis of the significant negative implications of CI on quality of life and its overwhelming association with poor outcomes, there is a compelling need for establishment of detailed consensus guidelines on cognitive screening methods to be systematically implemented in the population of patients with heart failure (HF). Since limited attention has been drawn exclusively on the field of CI in AHF thus far, the present narrative review aims to shed further light on the topic. The underlying pathophysiological mechanisms of CI in AHF remain poorly understood and seem to be multifactorial. Different pathophysiological pathways may come into play, depending on the clinical phenotype of AHF. There is some evidence that cognitive decline closely follows the perturbations incurred across the long-term disease trajectory of HF, both along the time course of stable chronic HF as well as during episodes of HF exacerbation. CI in AHF remains a rather under recognized scientific field that poses many challenges, since there are still many unresolved issues regarding cognitive changes in patients hospitalized with AHF that need to be thoroughly addressed. © 2021 by the authors. Licensee MDPI, Basel, Switzerland. LA - English DB - MTMT ER - TY - JOUR AU - Wang, M. AU - Hong, J.-C. AU - Zhou, F.-F. AU - Li, P.-C. TI - Application of laser speckle contrast imaging in the research on brain science JF - PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS J2 - PROG BIOCHEM BIOPHYS VL - 48 PY - 2021 IS - 8 SP - 922 EP - 937 PG - 16 SN - 1000-3282 DO - 10.16476/j.pibb.2021.0011 UR - https://m2.mtmt.hu/api/publication/32236169 ID - 32236169 AB - Laser speckle contrast imaging (LSCI) is a powerful and simple non-scanning real-time hemodynamic imaging method, with the advantages of high spatial and temporal resolution, wide imaging field, high-speed imaging, low damage, relatively simple instrument structure. After decades of development, it already has had the ability to quantify flow changes with higher resolution. Although LSCI is limited to superficial tissue imaging due to the limitation of depth resolution, it has been playing an important role in the studies and clinical applications of biomedical fields such as dermatology and neurological disease research. This paper briefly introduces the basic principle, typical device and technical progress of LSCI, and reviews the recent progress in brain diseases such as stroke, drug addiction, Alzheimer's disease and other applications of brain science. Finally, we discuss the prospects for development of LSCI in the study of brain science. © 2021 Institute of Biophysics,Chinese Academy of Sciences. All rights reserved. LA - Chinese DB - MTMT ER - TY - JOUR AU - Balasubramanian, P. AU - DelFavero, J. AU - Ungvári, Anna Sára AU - Papp, Magor Csongor AU - Tarantini, A. AU - Price, N. AU - de, Cabo R. AU - Tarantini, Stefano TI - Time-restricted feeding (TRF) for prevention of age-related vascular cognitive impairment and dementia JF - AGEING RESEARCH REVIEWS J2 - AGEING RES REV VL - 64 PY - 2020 PG - 9 SN - 1568-1637 DO - 10.1016/j.arr.2020.101189 UR - https://m2.mtmt.hu/api/publication/31623573 ID - 31623573 LA - English DB - MTMT ER - TY - JOUR AU - Bateman, G.A. AU - Lechner-Scott, J. AU - Bateman, A.R. AU - Attia, J. AU - Lea, R.A. TI - The Incidence of Transverse Sinus Stenosis in Multiple Sclerosis: Further Evidence of Pulse Wave Encephalopathy JF - MULTIPLE SCLEROSIS AND RELATED DISORDERS J2 - MULT SCLER RELAT DIS VL - 46 PY - 2020 PG - 8 SN - 2211-0348 DO - 10.1016/j.msard.2020.102524 UR - https://m2.mtmt.hu/api/publication/31624027 ID - 31624027 LA - English DB - MTMT ER - TY - JOUR AU - De, Oliveira J. AU - Engel, D.F. AU - De, Paula G.C. AU - Dos, Santos D.B. AU - Lopes, J.B. AU - Farina, M. AU - Moreira, E.L.G. AU - De, Bem A.F. TI - High Cholesterol Diet Exacerbates Blood-Brain Barrier Disruption in LDLr-/- Mice: Impact on Cognitive Function JF - JOURNAL OF ALZHEIMER'S DISEASE J2 - J ALZHEIMERS DIS VL - 78 PY - 2020 IS - 1 SP - 97 EP - 115 PG - 19 SN - 1387-2877 DO - 10.3233/JAD-200541 UR - https://m2.mtmt.hu/api/publication/31669070 ID - 31669070 AB - Background: Evidence has revealed an association between familial hypercholesterolemia and cognitive impairment. In this regard, a connection between cognitive deficits and hippocampal blood-brain barrier (BBB) breakdown was found in low-density lipoprotein receptor knockout mice (LDLr-/-), a mouse model of familial hypercholesterolemia. Objective: Herein we investigated the impact of a hypercholesterolemic diet on cognition and BBB function in C57BL/6 wild-type and LDLr-/-mice. Methods: Animals were fed with normal or high cholesterol diets for 30 days. Thus, wild-type and LDLr-/-mice were submitted to memory paradigms. Additionally, BBB integrity was evaluated in the mice's prefrontal cortices and hippocampi. Results: A tenfold elevation in plasma cholesterol levels of LDLr-/-mice was observed after a hypercholesterolemic diet, while in wild-type mice, the hypercholesterolemic diet exposure increased plasma cholesterol levels only moderately and did not induce cognitive impairment. LDLr-/-mice presented memory impairment regardless of the diet. We observed BBB disruption as an increased permeability to sodium fluorescein in the prefrontal cortices and hippocampi and a decrease on hippocampal claudin-5 and occludin mRNA levels in both wild-type and LDLr-/-mice treated with a hypercholesterolemic diet. The LDLr-/-mice fed with a regular diet already presented BBB dysfunction. The BBB-increased leakage in the hippocampi of LDLr-/-mice was related to high microvessel content and intense astrogliosis, which did not occur in the control mice. Conclusion: Therefore, LDLr-/-mice seem to be more susceptible to cognitive impairments and BBB damage induced by exposure to a high cholesterol diet. Finally, BBB disruption appears to be a relevant event in hypercholesterolemia-induced brain alterations. © 2020 - IOS Press and the authors. All rights reserved. LA - English DB - MTMT ER - TY - JOUR AU - Hill, L.K. AU - Hoang, D.M. AU - Chiriboga, L.A. AU - Wisniewski, T. AU - Sadowski, M.J. AU - Wadghiri, Y.Z. TI - Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography JF - FRONTIERS IN AGING NEUROSCIENCE J2 - FRONT AGING NEUROSCI VL - 12 PY - 2020 SN - 1663-4365 DO - 10.3389/fnagi.2020.585218 UR - https://m2.mtmt.hu/api/publication/31669068 ID - 31669068 AB - Microvascular rarefaction, or the decrease in vascular density, has been described in the cerebrovasculature of aging humans, rats, and, more recently, mice in the presence and absence of age-dependent diseases. Given the wide use of mice in modeling age-dependent human diseases of the cerebrovasculature, visualization, and quantification of the global murine cerebrovasculature is necessary for establishing the baseline changes that occur with aging. To provide in vivo whole-brain imaging of the cerebrovasculature in aging C57BL/6 mice longitudinally, contrast-enhanced magnetic resonance angiography (CE-MRA) was employed using a house-made gadolinium-bearing micellar blood pool agent. Enhancement in the vascular space permitted quantification of the detectable, or apparent, cerebral blood volume (aCBV), which was analyzed over 2 years of aging and compared to histological analysis of the cerebrovascular density. A significant loss in the aCBV was detected by CE-MRA over the aging period. Histological analysis via vessel-probing immunohistochemistry confirmed a significant loss in the cerebrovascular density over the same 2-year aging period, validating the CE-MRA findings. While these techniques use widely different methods of assessment and spatial resolutions, their comparable findings in detected vascular loss corroborate the growing body of literature describing vascular rarefaction aging. These findings suggest that such age-dependent changes can contribute to cerebrovascular and neurodegenerative diseases, which are modeled using wild-type and transgenic laboratory rodents. © Copyright © 2020 Hill, Hoang, Chiriboga, Wisniewski, Sadowski and Wadghiri. LA - English DB - MTMT ER - TY - JOUR AU - Kiss, Tamás AU - Nyúl-Tóth, Ádám AU - Balasubramanian, Priya AU - Tarantini, Stefano AU - Ahire, Chetan AU - Yabluchanskiy, Andriy AU - Csípő, Tamás AU - Farkas, Eszter AU - Wren, Jonathan D. AU - Garman, Lori AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Nicotinamide mononucleotide (NMN) supplementation promotes neurovascular rejuvenation in aged mice: transcriptional footprint of SIRT1 activation, mitochondrial protection, anti-inflammatory, and anti-apoptotic effects JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 42 PY - 2020 IS - 2 SP - 527 EP - 546 PG - 20 SN - 2509-2715 DO - 10.1007/s11357-020-00165-5 UR - https://m2.mtmt.hu/api/publication/31268883 ID - 31268883 N1 - Export Date: 3 April 2024 AB - Aging-induced structural and functional alterations of the neurovascular unit lead to impairment of neurovascular coupling responses, dysregulation of cerebral blood flow, and increased neuroinflammation, all of which contribute importantly to the pathogenesis of age-related vascular cognitive impairment (VCI). There is increasing evidence showing that a decrease in NAD(+) availability with age plays a critical role in age-related neurovascular and cerebromicrovascular dysfunction. Our recent studies demonstrate that restoring cellular NAD(+) levels in aged mice rescues neurovascular function, increases cerebral blood flow, and improves performance on cognitive tasks. To determine the effects of restoring cellular NAD(+) levels on neurovascular gene expression profiles, 24-month-old C57BL/6 mice were treated with nicotinamide mononucleotide (NMN), a key NAD(+) intermediate, for 2 weeks. Transcriptome analysis of preparations enriched for cells of the neurovascular unit was performed by RNA-seq. Neurovascular gene expression signatures in NMN-treated aged mice were compared with those in untreated young and aged control mice. We identified 590 genes differentially expressed in the aged neurovascular unit, 204 of which are restored toward youthful expression levels by NMN treatment. The transcriptional footprint of NMN treatment indicates that increased NAD(+) levels promote SIRT1 activation in the neurovascular unit, as demonstrated by analysis of upstream regulators of differentially expressed genes as well as analysis of the expression of known SIRT1-dependent genes. Pathway analysis predicts that neurovascular protective effects of NMN are mediated by the induction of genes involved in mitochondrial rejuvenation, anti-inflammatory, and anti-apoptotic pathways. In conclusion, the recently demonstrated protective effects of NMN treatment on neurovascular function can be attributed to multifaceted sirtuin-mediated anti-aging changes in the neurovascular transcriptome. Our present findings taken together with the results of recent studies using mitochondria-targeted interventions suggest that mitochondrial rejuvenation is a critical mechanism to restore neurovascular health and improve cerebral blood flow in aging. LA - English DB - MTMT ER - TY - JOUR AU - Kiss, Tamás AU - Nyúl-Tóth, Ádám AU - Balasubramanian, Priya AU - Tarantini, Stefano AU - Ahire, Chetan AU - DelFavero, Jordan AU - Yabluchanskiy, Andriy AU - Csípő, Tamás AU - Farkas, Eszter AU - Wiley, Graham AU - Garman, Lori AU - Csiszar, Anna AU - Ungvári, Zoltán István TI - Single-cell RNA sequencing identifies senescent cerebromicrovascular endothelial cells in the aged mouse brain JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 42 PY - 2020 IS - 2 SP - 429 EP - 444 PG - 16 SN - 2509-2715 DO - 10.1007/s11357-020-00177-1 UR - https://m2.mtmt.hu/api/publication/31281265 ID - 31281265 N1 - Export Date: 3 April 2024 AB - Age-related phenotypic changes of cerebromicrovascular endothelial cells lead to dysregulation of cerebral blood flow and blood-brain barrier disruption, promoting the pathogenesis of vascular cognitive impairment (VCI). In recent years, endothelial cell senescence has emerged as a potential mechanism contributing to microvascular pathologies opening the avenue to the therapeutic exploitation of senolytic drugs in preclinical studies. However, difficulties with the detection of senescent endothelial cells in wild type mouse models of aging hinder the assessment of the efficiency of senolytic treatments. To detect senescent endothelial cells in the aging mouse brain, we analyzed 4233 cells in fractions enriched for cerebromicrovascular endothelial cells and other cells associated with the neurovascular unit obtained from young (3-month-old) and aged (28-month-old) C57BL/6 mice. We define 13 transcriptomic cell types by deep, single-cell RNA sequencing. We match transcriptomic signatures of cellular senescence to endothelial cells identified on the basis of their gene expression profile. Our study demonstrates that with advanced aging, there is an increased ratio of senescent endothelial cells (similar to 10%) in the mouse cerebral microcirculation. We propose that our single-cell RNA sequencing-based method can be adapted to study the effect of aging on senescence in various brain cell types as well as to evaluate the efficiency of various senolytic regimens in multiple tissues. LA - English DB - MTMT ER - TY - JOUR AU - Rutkai, I. AU - Evans, W.R. AU - Bess, N. AU - Salter-Cid, T. AU - Cikic, S. AU - Chandra, P.K. AU - Katakam, P.V.G. AU - Mostany, R. AU - Busija, D.W. TI - Chronic imaging of mitochondria in the murine cerebral vasculature using in vivo two-photon microscopy JF - AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY J2 - AM J PHYSIOL HEART C VL - 318 PY - 2020 IS - 6 SP - H1379 EP - H1386 SN - 0363-6135 DO - 10.1152/ajpheart.00751.2019 UR - https://m2.mtmt.hu/api/publication/31349701 ID - 31349701 N1 - Department of Pharmacology, Tulane University School of Medicine, New Orleans, LA, United States Tulane Brain Institute, Tulane University, New Orleans, LA, United States Cited By :6 Export Date: 28 February 2024 CODEN: AJPPD Correspondence Address: Rutkai, I.; Department of Pharmacology, United States; email: irutkai@tulane.edu LA - English DB - MTMT ER - TY - JOUR AU - Thelen, M. AU - Brown-Borg, H.M. TI - Does Diet Have a Role in the Treatment of Alzheimer's Disease? JF - FRONTIERS IN AGING NEUROSCIENCE J2 - FRONT AGING NEUROSCI VL - 12 PY - 2020 SN - 1663-4365 DO - 10.3389/fnagi.2020.617071 UR - https://m2.mtmt.hu/api/publication/31818613 ID - 31818613 LA - English DB - MTMT ER - TY - JOUR AU - Uryash, A. AU - Flores, V. AU - Adams, J.A. AU - Allen, P.D. AU - Lopez, J.R. TI - Memory and Learning Deficits Are Associated With Ca2+ Dyshomeostasis in Normal Aging JF - FRONTIERS IN AGING NEUROSCIENCE J2 - FRONT AGING NEUROSCI VL - 12 PY - 2020 SN - 1663-4365 DO - 10.3389/fnagi.2020.00224 UR - https://m2.mtmt.hu/api/publication/31400542 ID - 31400542 LA - English DB - MTMT ER - TY - JOUR AU - Verheggen, Inge C. M. AU - de Jong, Joost J. A. AU - van Boxtel, Martin P. J. AU - Gronenschild, Ed H. B. M. AU - Palm, Walter M. AU - Postma, Alida A. AU - Jansen, Jacobus F. A. AU - Verhey, Frans R. J. AU - Backes, Walter H. TI - Increase in blood-brain barrier leakage in healthy, older adults JF - GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE) J2 - GEROSCIENCE VL - 42 PY - 2020 IS - 4 SP - 1183 EP - 1193 PG - 11 SN - 2509-2715 DO - 10.1007/s11357-020-00211-2 UR - https://m2.mtmt.hu/api/publication/31450313 ID - 31450313 N1 - Export Date: 3 April 2024 AB - Blood-brain barrier (BBB) breakdown can disrupt nutrient supply and waste removal, which affects neuronal functioning. Currently, dynamic contrast-enhanced (DCE) MRI is the preferred in-vivo method to quantify BBB leakage. Dedicated DCE MRI studies in normal aging individuals are lacking, which could hamper value estimation and interpretation of leakage rate in pathological conditions. Therefore, we applied DCE MRI to investigate the association between BBB disruption and age in a healthy sample. Fifty-seven cognitively and neurologically healthy, middle-aged to older participants (mean age: 66 years, range: 47-91 years) underwent MRI, including DCE MRI with intravenous injection of a gadolinium-based contrast agent. Pharmacokinetic modeling was applied to contrast concentration time-curves to estimate BBB leakage rate in each voxel. Subsequently, leakage rate was calculated in the white and gray matter, and primary (basic sensory and motor functions), secondary (association areas), and tertiary (higher-order cognition) brain regions. A difference in vulnerability to deterioration was expected between these regions, with especially tertiary regions being affected by age. Higher BBB leakage rate was significantly associated with older age in the white and gray matter, and also in tertiary, but not in primary or secondary brain regions. Even in healthy individuals, BBB disruption was stronger in older persons, which suggests BBB disruption is a normal physiologically aging phenomenon. Age-related increase in BBB disruption occurred especially in brain regions most vulnerable to age-related deterioration, which may indicate that BBB disruption is an underlying mechanism of normal age-related decline. Netherlands Trial Register number: NL6358, date of registration: 2017-03-24. LA - English DB - MTMT ER - TY - JOUR AU - Wu, Y. AU - Wu, H. AU - Guo, X. AU - Pluimer, B. AU - Zhao, Z. TI - Blood–Brain Barrier Dysfunction in Mild Traumatic Brain Injury: Evidence From Preclinical Murine Models JF - FRONTIERS IN PHYSIOLOGY J2 - FRONT PHYSIOL VL - 11 PY - 2020 PG - 11 SN - 1664-042X DO - 10.3389/fphys.2020.01030 UR - https://m2.mtmt.hu/api/publication/31624028 ID - 31624028 LA - English DB - MTMT ER - TY - JOUR AU - Yabluchanskiy, A. AU - Balasubramanian, P. AU - Tarantini, Stefano TI - Cerebrovascular Rejuvenation: Novel Strategies for Prevention of Vascular Cognitive Impairment JF - REJUVENATION RESEARCH J2 - REJUV RES VL - 23 PY - 2020 IS - 6 SP - 451 EP - 452 PG - 2 SN - 1549-1684 DO - 10.1089/rej.2020.2402 UR - https://m2.mtmt.hu/api/publication/31795478 ID - 31795478 LA - English DB - MTMT ER - TY - JOUR AU - Yang, Jie AU - Ma, Kui AU - Zhang, Cuiping AU - Liu, Yufan AU - Liang, Feng AU - Hu, Wenzhi AU - Bian, Xiaowei AU - Yang, Siming AU - Fu, Xiaobing TI - Burns Impair Blood-Brain Barrier and Mesenchymal Stem Cells Can Reverse the Process in Mice JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 11 PY - 2020 PG - 13 SN - 1664-3224 DO - 10.3389/fimmu.2020.578879 UR - https://m2.mtmt.hu/api/publication/31692956 ID - 31692956 AB - Neurological syndromes are observed in numerous patients who suffer burns, which add to the economic burden of societies and families. Recent studies have implied that blood-brain barrier (BBB) dysfunction is the key factor that induces these central nervous system (CNS) syndromes in peripheral traumatic disease, e.g., surgery and burns. However, the effect of burns on BBB and the underlying mechanism remains, largely, to be determined. The present study aimed to investigate the effect of burns on BBB and the potential of umbilical cord-derived mesenchymal stem cells (UC-MSCs), which have strong anti-inflammatory and repairing ability, to protect the integrity of BBB. BBB permeability was evaluated using dextran tracer (immunohistochemistry imaging and spectrophotometric quantification) and western blot, interleukin (IL)-6, and IL-1 beta levels in blood and brain were measured by enzyme-linked immunosorbent assay. Furthermore, transmission electron microscopy (TEM) was used to detect transcellular vesicular transport (transcytosis) in BBB. We found that burns increased mouse BBB permeability to both 10-kDa and 70-kDa dextran. IL-6 and IL-1 beta levels increased in peripheral blood and CNS after burns. In addition, burns decreased the level of tight junction proteins (TJs), including claudin-5, occludin, and ZO-1, which indicated increased BBB permeability due to paracellular pathway. Moreover, increased vesicular density after burns suggested increased transcytosis in brain microvascular endothelial cells. Finally, administering UC-MSCs at 1 h after burns effectively reversed these adverse effects and protected the integrity of BBB. These results suggest that burns increase BBB permeability through both paracellular pathway and transcytosis, the potential mechanism of which might be through increasing IL-6 and IL-1 beta levels and decreasing Mfsd2a level, and appropriate treatment with UC-MSCs can reverse these effects and protect the integrity of BBB after burns. LA - English DB - MTMT ER -