@article{MTMT:34525861,
	title = {Chronic fatigue syndrome and multiple sclerosis have reduced craniospinal compliance and dilated pressurized bridging cortical veins},
	url = {https://m2.mtmt.hu/api/publication/34525861},
	author = {Bateman, G.A. and Bateman, A.R.},
	doi = {10.1016/j.mehy.2023.111243},
	journal-iso = {MED HYPOTHESES},
	journal = {MEDICAL HYPOTHESES},
	volume = {182},
	unique-id = {34525861},
	issn = {0306-9877},
	abstract = {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},
	keywords = {Adult; Female; Middle Aged; Male; ARTICLE; SUPERIOR SAGITTAL SINUS; human; case report; clinical article; Insomnia; Young Adult; headache; MULTIPLE SCLEROSIS; MULTIPLE SCLEROSIS; Epstein Barr virus; Subarachnoid Space; myalgia; Venous Pressure; Venous Pressure; pharyngitis; malaise; photosensitivity; pulse wave; pressure gradient; hypothesis; Vein; tonsillitis; Neck Pain; walking difficulty; dysesthesia; muscle twitch; hand paresthesia; disorders of higher cerebral function; brain vein; chronic fatigue syndrome; chronic fatigue syndrome; limb weakness; Myalgic encephalomyelitis; cranial sinus; cerebrospinal fluid pressure; T1 weighted imaging; vertebral canal; Cortical vein; bridging cortical vein; spinal stiffness},
	year = {2024},
	eissn = {1532-2777}
}

@article{MTMT:34444878,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/34444878},
	author = {Gulej, Rafal and Csik, B. and Faakye, J. and Tarantini, Stefano and Shanmugarama, S. and Chandragiri, S.S. and Mukli, P. and Conley, S. and Csiszar, Anna and Ungvári, Zoltán István and Yabluchanskiy, A. and Nyúl-Tóth, Ádám},
	doi = {10.1111/micc.12840},
	journal-iso = {MICROCIRCULATION},
	journal = {MICROCIRCULATION},
	volume = {31},
	unique-id = {34444878},
	issn = {1073-9688},
	year = {2024},
	eissn = {1549-8719},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34474845,
	title = {Rejuvenation of cerebromicrovascular function in aged mice through heterochronic parabiosis: insights into neurovascular coupling and the impact of young blood factors},
	url = {https://m2.mtmt.hu/api/publication/34474845},
	author = {Gulej, R. and Nyúl-Tóth, Ádám and Csik, B. and Petersen, B. and Faakye, J. and Negri, S. and Chandragiri, S.S. and Mukli, Péter and Yabluchanskiy, A. and Conley, S. and Huffman, D.M. and Csiszar, Anna and Tarantini, Stefano and Ungvári, Zoltán István},
	doi = {10.1007/s11357-023-01039-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {46},
	unique-id = {34474845},
	issn = {2509-2715},
	year = {2024},
	eissn = {2509-2723},
	pages = {327-347},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34729965,
	title = {IGF1R deficiency in vascular smooth muscle cells impairs myogenic autoregulation and cognition in mice},
	url = {https://m2.mtmt.hu/api/publication/34729965},
	author = {Miller, L.R. and Bickel, M.A. and Tarantini, S. and Runion, M.E. and Matacchiera, Z. and Vance, M.L. and Hibbs, C. and Vaden, H. and Nagykaldi, D. and Martin, T. and Bullen, E.C. and Pinckard, J. and Kiss, Tamás and Howard, E.W. and Yabluchanskiy, A. and Conley, S.M.},
	doi = {10.3389/fnagi.2024.1320808},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {16},
	unique-id = {34729965},
	issn = {1663-4365},
	year = {2024},
	eissn = {1663-4365},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227}
}

@article{MTMT:34775693,
	title = {Clinicoradiological Features and Long-term Cognitive and Functional Outcome in Patients with Deep Cerebral Venous Thrombosis},
	url = {https://m2.mtmt.hu/api/publication/34775693},
	author = {Patwardhan, A. and Gupta, M. and Philip, M. and Rangarajan, A. and Joshi, T. and Alladi, S. and Kulkarni, G.B. and Ramakrishnan, S.},
	doi = {10.4103/aian.aian_792_23},
	journal-iso = {ANN INDIAN ACAD NEUR},
	journal = {ANNALS OF INDIAN ACADEMY OF NEUROLOGY},
	volume = {27},
	unique-id = {34775693},
	issn = {0972-2327},
	abstract = {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.},
	keywords = {Adult; Female; Male; ARTICLE; DEMENTIA; DEPRESSION; APHASIA; neurologic disease; human; medical record; computer assisted tomography; nuclear magnetic resonance imaging; phenytoin; clinical article; cognition; ANEMIA; human immunodeficiency virus; vomiting; headache; neuropsychology; seizure; HEMIPARESIS; telemedicine; cognitive defect; mini mental state examination; anticoagulant agent; levetiracetam; functional assessment; CEREBRAL VENOUS THROMBOSIS; VASCULAR DEMENTIA; hospital service; Demographics; sensory system; mortality rate; Addenbrooke Cognitive Examination; cerebral sinus thrombosis; NEUROPSYCHOLOGICAL ASSESSMENT; Cognitive screening; Patient Health Questionnaire 9; psychiatric department; B12 deficiency; coronavirus disease 2019; TICS-M},
	year = {2024},
	eissn = {1998-3549},
	pages = {34-39}
}

@article{MTMT:34525203,
	title = {Impact of knockout of dual-specificity protein phosphatase 5 on structural and mechanical properties of rat middle cerebral arteries: implications for vascular aging},
	url = {https://m2.mtmt.hu/api/publication/34525203},
	author = {Tang, C. and Zhang, H. and Border, J.J. and Liu, Y. and Fang, X. and Jefferson, J.R. and Gregory, A. and Johnson, C. and Lee, T.J. and Bai, S. and Sharma, A. and Shin, S.M. and Yu, H. and Roman, R.J. and Fan, F.},
	doi = {10.1007/s11357-024-01061-y},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {in press},
	unique-id = {34525203},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {PKC; ERK; Vascular mechanical properties; DUSP5; AD/ADRD},
	year = {2024},
	eissn = {2509-2723}
}

@article{MTMT:34775692,
	title = {Cerebral venous impairment and cerebral venous sinus thrombosis},
	url = {https://m2.mtmt.hu/api/publication/34775692},
	author = {Wang, J. and Manaenko, A. and Hu, Q. and Zhang, X.},
	doi = {10.1016/j.hest.2024.03.002},
	journal-iso = {BRAIN HEMORRHAGES},
	journal = {BRAIN HEMORRHAGES},
	volume = {in press},
	unique-id = {34775692},
	abstract = {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},
	keywords = {Cerebral Veins; NEUROLOGICAL DISEASES; cerebral venous sinus thrombosis (cvst); Imaging-based evaluation},
	year = {2024},
	eissn = {2589-238X}
}

@article{MTMT:34396778,
	title = {Cognitive impairment in cerebral small vessel disease induced by hypertension},
	url = {https://m2.mtmt.hu/api/publication/34396778},
	author = {Wei, Weipeng and Ma, Denglei and Li, Lin and Zhang, Lan},
	doi = {10.4103/1673-5374.385841},
	journal-iso = {NEUR REG RES},
	journal = {NEURAL REGENERATION RESEARCH},
	volume = {19},
	unique-id = {34396778},
	issn = {1673-5374},
	abstract = {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.},
	year = {2024},
	eissn = {1876-7958},
	pages = {1454-1462},
	orcid-numbers = {Zhang, Lan/0000-0003-0740-6751}
}

@article{MTMT:34055636,
	title = {Dilatation of the bridging cerebral veins in multiple sclerosis correlates with fatigue and suggests an increase in pressure},
	url = {https://m2.mtmt.hu/api/publication/34055636},
	author = {Bateman, G.A. and Bateman, A.R. and Lechner-Scott, J.},
	doi = {10.1016/j.msard.2023.104843},
	journal-iso = {MULT SCLER RELAT DIS},
	journal = {MULTIPLE SCLEROSIS AND RELATED DISORDERS},
	volume = {76},
	unique-id = {34055636},
	issn = {2211-0348},
	abstract = {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},
	keywords = {fatigue; MULTIPLE SCLEROSIS; Venous Pressure; Cortical vein area},
	year = {2023},
	eissn = {2211-0356}
}

@article{MTMT:34525862,
	title = {Pressure-support compared with pressure-controlled ventilation mitigates lung and brain injury in experimental acute ischemic stroke in rats},
	url = {https://m2.mtmt.hu/api/publication/34525862},
	author = {da, Silva A.L. and Bessa, C.M. and Rocha, N.N. and Carvalho, E.B. and Magalhaes, R.F. and Capelozzi, V.L. and Robba, C. and Pelosi, P. and Samary, C.S. and Rocco, P.R.M. and Silva, P.L.},
	doi = {10.1186/s40635-023-00580-w},
	journal-iso = {INTENSIVE CARE MED EXP},
	journal = {INTENSIVE CARE MEDICINE EXPERIMENTAL},
	volume = {11},
	unique-id = {34525862},
	abstract = {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).},
	keywords = {Male; Inflammation; THROMBOSIS; immunohistochemistry; hippocampus; NECROSIS; ARTICLE; controlled study; nonhuman; animal tissue; animal model; animal experiment; disease severity; Histology; randomized controlled trial; Experimental study; biological marker; somatosensory cortex; dentate gyrus; brain tissue; BLOOD GAS ANALYSIS; Hemodynamics; Tidal Volume; Heart Rate; Echocardiography; systolic blood pressure; prospective study; edema; mean arterial pressure; heart output; KETAMINE; LUNG INJURY; LUNG INJURY; laparotomy; microglia; Molecular Biology; midazolam; interleukin 1beta; Choroid Plexus; blood brain barrier; bleeding; internal carotid artery; claudin 5; artificial ventilation; brain injury; brain injury; Acute ischemic stroke; Acute ischemic stroke; mononuclear phagocyte; transthoracic echocardiography; Mechanical ventilation; Tracheostomy; protein ZO1; Lung mechanics; arterial blood; heart left ventricle endsystolic volume; brain histology; neuropil; receptor type tyrosine protein phosphatase C; heart right ventricle endsystolic volume; xylazine; rat; Pressure support ventilation; atelectasis; airway pressure; peak systolic velocity; experimental cerebral ischemia; pancuronium bromide; thermocoagulation; low tidal volume ventilation; Diffuse alveolar damage; Brain necrosis; Fraction of inspired oxygen; positive end expiratory pressure ventilation; pressure controlled ventilation},
	year = {2023},
	eissn = {2197-425X}
}

@article{MTMT:33688898,
	title = {Blood tissue Plasminogen Activator (tPA) of liver origin contributes to neurovascular coupling involving brain endothelial N-Methyl-D-Aspartate (NMDA) receptors},
	url = {https://m2.mtmt.hu/api/publication/33688898},
	author = {Furon, J. and Yetim, M. and Pouettre, E. and Martinez, de Lizarrondo S. and Maubert, E. and Hommet, Y. and Lebouvier, L. and Zheng, Z. and Ali, C. and Vivien, D.},
	doi = {10.1186/s12987-023-00411-w},
	journal-iso = {FLUIDS BARRIERS CNS},
	journal = {FLUIDS AND BARRIERS OF THE CNS},
	volume = {20},
	unique-id = {33688898},
	issn = {2045-8118},
	abstract = {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).},
	keywords = {Brain; Brain; Animals; Male; metabolism; LIVER; LIVER; LIVER; MICE; ARTICLE; MOUSE; animal; controlled study; nonhuman; animal tissue; animal experiment; animal cell; regulatory mechanism; n methyl dextro aspartic acid receptor; n methyl dextro aspartic acid receptor; Mice, Knockout; Hepatectomy; hydrodynamics; normal value; enzyme deficiency; enzyme blood level; endothelium cell; liver cell; endothelial cells; vascular endothelium; knockout mouse; Receptors, N-Methyl-D-Aspartate; enzyme release; bradykinin B2 receptor; enzyme synthesis; N-Methylaspartate; n methylaspartic acid; Tissue Plasminogen Activator; Tissue Plasminogen Activator; Tissue Plasminogen Activator; TPA; Neurovascular coupling; Neurovascular coupling; NMDAR; vascular endothelial cadherin; PARABIOSIS; GluN1; Cre recombinase; tissue plasminogen activator blood level; NVC},
	year = {2023},
	eissn = {2045-8118}
}

@article{MTMT:34399032,
	title = {Chinese expert consensus on the diagnosis and treatment of venous reflux disorders of head and neck},
	url = {https://m2.mtmt.hu/api/publication/34399032},
	author = {Ji, X.},
	doi = {10.3760/cma.j.cn112137-20230112-00069},
	journal-iso = {NAT MED J CHINA},
	journal = {NATIONAL MEDICAL JORNAL OF CHINA/CHINESE MEDICAL JOURNAL},
	volume = {103},
	unique-id = {34399032},
	issn = {0376-2491},
	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. © 2023 Chinese Medical Association. All rights reserved.},
	keywords = {Humans; human; cerebrovascular accident; Constriction, Pathologic; Consensus; Consensus; Cerebrovascular Disorders; stroke; Neck; Neck; head; head; stenosis, occlusion and obstruction; Intracranial Hypertension; Jugular Veins; jugular vein; EXPERT CONSENSUS; cerebral venous sinus thrombosis; Cerebral venous diseases; Internal jugular venous stenosis; Venous reflux disorders of head and neck},
	year = {2023},
	pages = {1257-1279}
}

@article{MTMT:34399031,
	title = {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},
	url = {https://m2.mtmt.hu/api/publication/34399031},
	author = {Ko, W. and Baek, J.-S. and Liu, Z. and Dong, L. and Kim, N. and Lee, H. and Yoon, C.-S. and Kim, N.Y. and Kim, S.C. and Lee, D.-S.},
	doi = {10.3390/molecules28217299},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {28},
	unique-id = {34399031},
	issn = {1420-3049},
	abstract = {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.},
	keywords = {metabolism; PAIN; PAIN; signal transduction; signal transduction; LIPOPOLYSACCHARIDE; Cyclooxygenase 2; Cyclooxygenase 2; Anti-Inflammatory Agents; interleukin 6; Lipopolysaccharides; nitric oxide; nitric oxide; antiinflammatory agent; mitogen activated protein kinase; microglia; microglia; Nitric Oxide Synthase Type II; NF-kappa B; immunoglobulin enhancer binding protein; Interleukin-6; inducible nitric oxide synthase; Mitogen-Activated Protein Kinases; Moraceae; Moraceae; 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone; 1,6,7-Trihydroxy-2-(1,1-dimethyl-2-propenyl)-3-methoxyxanthone; mouse macrophage RAW 264.7; mouse microglia BV2},
	year = {2023},
	eissn = {1420-3049}
}

@article{MTMT:34208621,
	title = {Fetal head-down posture may explain the rapid brain evolution in humans and other primates: An interpretative review},
	url = {https://m2.mtmt.hu/api/publication/34208621},
	author = {Macionis, V.},
	doi = {10.1016/j.brainres.2023.148558},
	journal-iso = {BRAIN RES},
	journal = {BRAIN RESEARCH},
	volume = {1820},
	unique-id = {34208621},
	issn = {0006-8993},
	abstract = {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.},
	keywords = {Brain; PHYLOGENY; review; review; human; HYPERTENSION; Haplorhini; nonhuman; Hydrostatic pressure; nuclear magnetic resonance imaging; PRIMATE; Hemodynamics; fetus blood; body mass; brain blood flow; blood flow; AUTOREGULATION; CIRCULATION; APE; brain circulation; brain development; Head-Down Tilt; sitting; neocortex; brain size; venous circulation; head circumference; brain evolution; physiological process; postnatal growth; brain growth; Elephant; encephalization; cephalopelvic disproportion; simian; Anthropoids; Cephalopelvic proportions; Fetal postural hemodynamics; fossil hominin},
	year = {2023},
	eissn = {1872-6240}
}

@article{MTMT:34039837,
	title = {The pathophysiology of cognitive impairment in individuals with heart failure: a systematic review},
	url = {https://m2.mtmt.hu/api/publication/34039837},
	author = {Ni, R.S.S. and Mohamed, Raffi H.Q. and Dong, Y.},
	doi = {10.3389/fcvm.2023.1181979},
	journal-iso = {FRONT CARDIOVASC MED},
	journal = {FRONTIERS IN CARDIOVASCULAR MEDICINE},
	volume = {10},
	unique-id = {34039837},
	issn = {2297-055X},
	abstract = {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.},
	keywords = {PATHOPHYSIOLOGY; DEMENTIA; heart failure; systematic review; COGNITIVE IMPAIRMENT},
	year = {2023},
	eissn = {2297-055X}
}

@article{MTMT:34252131,
	title = {The Role of Methionine-Rich Diet in Unhealthy Cerebrovascular and Brain Aging: Mechanisms and Implications for Cognitive Impairment},
	url = {https://m2.mtmt.hu/api/publication/34252131},
	author = {Ungvári, Anna Sára and Gulej, Rafal and Csik, Boglarka and Mukli, Péter and Negri, Sharon and Tarantini, Stefano and Yabluchanskiy, Andriy and Benyó, Zoltán and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.3390/nu15214662},
	journal-iso = {NUTRIENTS},
	journal = {NUTRIENTS},
	volume = {15},
	unique-id = {34252131},
	abstract = {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.},
	year = {2023},
	eissn = {2072-6643},
	orcid-numbers = {Gulej, Rafal/0000-0002-9958-707X; Mukli, Péter/0000-0003-4355-8103; Tarantini, Stefano/0000-0001-5627-1430; Benyó, Zoltán/0000-0001-6015-0359; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34055638,
	title = {Cerebral venous congestion alters brain metabolite profiles, impairing cognitive function},
	url = {https://m2.mtmt.hu/api/publication/34055638},
	author = {Wei, H. and Jiang, H. and Zhou, Y. and Xiao, X. and Zhou, C. and Ji, X.},
	doi = {10.1177/0271678X231182244},
	journal-iso = {J CEREBR BLOOD F MET},
	journal = {JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM},
	volume = {43},
	unique-id = {34055638},
	issn = {0271-678X},
	abstract = {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.},
	keywords = {Cerebral circulation; Vein; vascular cognitive impairment (VCI); Vascular contributions to cognitive impairment and dementia (VCID); cerebral venous congestion},
	year = {2023},
	eissn = {1559-7016},
	pages = {1857-1872}
}

@article{MTMT:33551588,
	title = {Cognitive impairment in patients with heart failure: molecular mechanism and therapy},
	url = {https://m2.mtmt.hu/api/publication/33551588},
	author = {Wu, Y. and Chen, L. and Zhong, F. and Zhou, K. and Lu, C. and Cheng, X. and Wang, S.},
	doi = {10.1007/s10741-022-10289-9},
	journal-iso = {HEART FAIL REV},
	journal = {HEART FAILURE REVIEWS},
	volume = {28},
	unique-id = {33551588},
	issn = {1382-4147},
	abstract = {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.},
	keywords = {heart failure; treatment; COGNITIVE IMPAIRMENT; nursing; pathophysiological mechanism},
	year = {2023},
	eissn = {1573-7322},
	pages = {807-820}
}

@article{MTMT:32682118,
	title = {Quantified hemodynamic parameters of the venous system in multiple sclerosis: A systematic review},
	url = {https://m2.mtmt.hu/api/publication/32682118},
	author = {Bateman, A.R. and Lechner-Scott, J. and Barber, T. and Bateman, G.A. and Ramadan, S.},
	doi = {10.1016/j.msard.2021.103477},
	journal-iso = {MULT SCLER RELAT DIS},
	journal = {MULTIPLE SCLEROSIS AND RELATED DISORDERS},
	volume = {57},
	unique-id = {32682118},
	issn = {2211-0348},
	abstract = {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.},
	keywords = {MULTIPLE SCLEROSIS; Venous Pressure; Cerebral hemodynamics; Venous flow rate},
	year = {2022},
	eissn = {2211-0356}
}

@article{MTMT:32870866,
	title = {Identification of Potential Anti‐Neuroinflammatory Inhibitors from Antarctic Fungal Strain Aspergillus sp. SF‐7402 via Regulating the NF‐κB Signaling Pathway in Microglia},
	url = {https://m2.mtmt.hu/api/publication/32870866},
	author = {Cao, T.Q. and Liu, Z. and Dong, L. and Lee, H. and Ko, W. and Vinh, L.B. and Tuan, N.Q. and Kim, Y.-C. and Sohn, J.H. and Yim, J.H. and Lee, D.-S. and Oh, H.},
	doi = {10.3390/molecules27092851},
	journal-iso = {MOLECULES},
	journal = {MOLECULES},
	volume = {27},
	unique-id = {32870866},
	issn = {1420-3049},
	abstract = {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.},
	keywords = {neuroinflammation; ANTARCTICA; NF-κB; sterigmatocystin; BV2 cells; fungi metabolites},
	year = {2022},
	eissn = {1420-3049}
}

@article{MTMT:32590647,
	title = {Cerebral venous congestion exacerbates cerebral microhemorrhages in mice},
	url = {https://m2.mtmt.hu/api/publication/32590647},
	author = {Nyúl-Tóth, Ádám and Fülöp, Gábor Áron and Tarantini, Stefano and Kiss, Tamás and Ahire, Chetan and Faakye, Janet A and Ungvári, Anna Sára and Tóth, Péter József and Tóth, Attila and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-021-00504-0},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {44},
	unique-id = {32590647},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {heart failure; Cerebral circulation; Vein; Intracerebral hemorrhage; Microbleed; VCI; Vascular cognitive impairment; ICH; Venous congestion; Vascular contributions to cognitive impairment and dementia (VCID)},
	year = {2022},
	eissn = {2509-2723},
	pages = {805-816},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:33185900,
	title = {Pearls & Oy-sters: Cerebral Venous Congestion Associated With Cognitive Decline Treated by Jugular Release},
	url = {https://m2.mtmt.hu/api/publication/33185900},
	author = {Primiani, C.T. and Lawton, M. and Hillis, A.E. and Hui, F.K.},
	doi = {10.1212/WNL.0000000000201037},
	journal-iso = {NEUROLOGY},
	journal = {NEUROLOGY},
	volume = {99},
	unique-id = {33185900},
	issn = {0028-3878},
	abstract = {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.},
	keywords = {Male; Male; Humans; HYPEREMIA; HYPEREMIA; human; Quality of Life; Quality of Life; case report; Diagnostic Imaging; surgery; COGNITIVE DYSFUNCTION; cognitive defect; Jugular Veins; jugular vein; Cerebral Veins; brain vein},
	year = {2022},
	eissn = {1526-632X},
	pages = {577-580}
}

@inproceedings{MTMT:33599620,
	title = {Study on blood vessel segmentation of laser scattering microscopic image},
	url = {https://m2.mtmt.hu/api/publication/33599620},
	author = {Qu, B. and Rui, Z.},
	booktitle = {4th IEEE International Conference on Civil Aviation Safety and Information Technology, ICCASIT 2022},
	doi = {10.1109/ICCASIT55263.2022.9986646},
	unique-id = {33599620},
	abstract = {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.},
	keywords = {BLOOD; Image segmentation; Learning algorithms; Blood Vessels; image enhancement; Matched filter; Matched filters; Deep learning; Microscopic image; U-Net; U-Net; LSCI; Laser scattering; scatter imaging; Frangi filter; Frangi filter; Net networks; Vascular segmentations; adaptive contrast enhancement; adaptive contrast enhancement; Laser scatter imaging; Recurrent-U-net; Recurrent-U-net},
	year = {2022},
	pages = {1294-1299}
}

@article{MTMT:33025364,
	title = {Study on relationship between venous system and white matter hyperintensitiy in cerebral small vessel disease},
	url = {https://m2.mtmt.hu/api/publication/33025364},
	author = {Yijing, J. and Cancan, L. and Yuanxiao, W. and Liqun, F.},
	doi = {10.3760/cma.j.cn101721-20211021-000192},
	journal-iso = {CLINICAL MEDICINE OF CHINA},
	journal = {CLINICAL MEDICINE OF CHINA},
	volume = {38},
	unique-id = {33025364},
	issn = {1008-6315},
	abstract = {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.},
	keywords = {Cerebral Veins; white matter hyperintensity; Internal jugular vein},
	year = {2022},
	pages = {284-288}
}

@article{MTMT:31923447,
	title = {Obesity-induced cognitive impairment in older adults: a microvascular perspective},
	url = {https://m2.mtmt.hu/api/publication/31923447},
	author = {Balasubramanian, Priya and Kiss, Tamás and Tarantini, Stefano and Nyúl-Tóth, Ádám and Ahire, Chetan and Yabluchanskiy, Andriy and Csípő, Tamás and Lipécz, Ágnes and Tabák, Ádám and Institoris, Adam and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1152/ajpheart.00736.2020},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {320},
	unique-id = {31923447},
	issn = {0363-6135},
	abstract = {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.},
	keywords = {Aging; endothelial dysfunction; metabolic syndrome; senescence; Neurovascular coupling},
	year = {2021},
	eissn = {1522-1539},
	pages = {H740-H761},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Tabák, Ádám/0000-0002-6234-3936; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:31624021,
	title = {The central nervous system and heart failure},
	url = {https://m2.mtmt.hu/api/publication/31624021},
	author = {Dayer, Mark and MacIver, David H. and Rosen, Stuart D.},
	doi = {10.2217/fca-2020-0059},
	journal-iso = {FUTURE CARDIOL},
	journal = {FUTURE CARDIOLOGY},
	volume = {17},
	unique-id = {31624021},
	issn = {1479-6678},
	abstract = {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.},
	keywords = {CNS; CEREBRAL-BLOOD-FLOW; functional magnetic resonance imaging; Cognitive function; Valsalva maneuver; renin-angiotensin-aldosterone system; ALZHEIMER-DISEASE; cerebral blood flow; diffusion tensor imaging; ATRIAL-FIBRILLATION; CARDIAC-OUTPUT; Chronic heart failure; OLDER-ADULTS; Brain volume; WHITE-MATTER HYPERINTENSITIES; subclinical cerebral infarction},
	year = {2021},
	eissn = {1744-8298},
	pages = {363-382},
	orcid-numbers = {Dayer, Mark/0000-0002-0976-9743}
}

@article{MTMT:31836015,
	title = {Venous dysfunction plays a critical role in “normal” white matter disease of aging},
	url = {https://m2.mtmt.hu/api/publication/31836015},
	author = {Kapadia, A. and Dmytriw, A.A.},
	doi = {10.1016/j.mehy.2020.110457},
	journal-iso = {MED HYPOTHESES},
	journal = {MEDICAL HYPOTHESES},
	volume = {146},
	unique-id = {31836015},
	issn = {0306-9877},
	year = {2021},
	eissn = {1532-2777}
}

@article{MTMT:31907081,
	title = {Reduced pericyte and tight junction coverage in old diabetic rats are associated with hyperglycemia-induced cerebrovascular pericyte dysfunction},
	url = {https://m2.mtmt.hu/api/publication/31907081},
	author = {Liu, Y. and Zhang, H. and Wang, S. and Guo, Y. and Fang, X. and Zheng, B. and Gao, W. and Yu, H. and Chen, Z. and Roman, R.J. and Fan, F.},
	doi = {10.1152/AJPHEART.00726.2020},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {320},
	unique-id = {31907081},
	issn = {0363-6135},
	abstract = {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},
	keywords = {diabetes mellitus; Aging; Blood-Brain Barrier; Oxidative stress; Cerebral vascular pericytes},
	year = {2021},
	eissn = {1522-1539},
	pages = {H549-H562}
}

@article{MTMT:32558712,
	title = {Cefazolin Improves Anesthesia and Surgery-Induced Cognitive Impairments by Modulating Blood-Brain Barrier Function, Gut Bacteria and Short Chain Fatty Acids},
	url = {https://m2.mtmt.hu/api/publication/32558712},
	author = {Luo, A. and Li, S. and Wang, X. and Xie, Z. and Li, S. and Hua, D.},
	doi = {10.3389/fnagi.2021.748637},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {13},
	unique-id = {32558712},
	issn = {1663-4365},
	abstract = {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.},
	keywords = {Blood-Brain Barrier; CEFAZOLIN; gut microbiota; Short chain fatty acids; Postoperative cognitive dysfunction (POCD)},
	year = {2021},
	eissn = {1663-4365}
}

@article{MTMT:32505562,
	title = {The aging venous system: from varicosities to vascular cognitive impairment},
	url = {https://m2.mtmt.hu/api/publication/32505562},
	author = {Molnár, Andrea Ágnes and Nádasy, György László and Bednárikné Dörnyei, Gabriella and Patai, Bernadett Bettina and Delfavero, J. and Fülöp, Gábor Áron and Kirkpatrick, A.C. and Ungvári, Zoltán István and Merkely, Béla Péter},
	doi = {10.1007/s11357-021-00475-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {43},
	unique-id = {32505562},
	issn = {2509-2715},
	abstract = {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).},
	keywords = {Aging; Veins; Ageing; deep vein thrombosis; Venous Insufficiency; Varicose Veins; Vascular cognitive impairment; geroscience},
	year = {2021},
	eissn = {2509-2723},
	pages = {2761-2784},
	orcid-numbers = {Nádasy, György László/0000-0003-2057-2391; Bednárikné Dörnyei, Gabriella/0000-0001-7007-6252; Patai, Bernadett Bettina/0000-0003-1631-1607; Ungvári, Zoltán István/0000-0002-6035-6039; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:31963966,
	title = {Neurointenzív Tanszék – az első év},
	url = {https://m2.mtmt.hu/api/publication/31963966},
	author = {Molnár, Tihamér and Ezer, Erzsébet},
	journal-iso = {FOCUS MEDICINAE},
	journal = {FOCUS MEDICINAE},
	volume = {23},
	unique-id = {31963966},
	issn = {1419-0478},
	year = {2021},
	pages = {3-5}
}

@article{MTMT:31967308,
	title = {Demonstration of age-related blood-brain barrier disruption and cerebromicrovascular rarefaction in mice by longitudinal intravital two-photon microscopy and optical coherence tomography},
	url = {https://m2.mtmt.hu/api/publication/31967308},
	author = {Nyúl-Tóth, Ádám and Tarantini, Stefano and DelFavero, J. and Yan, F. and Balasubramanian, P. and Yabluchanskiy, A. and Ahire, C. and Kiss, Tamás and Csípő, Tamás and Lipécz, Ágnes and Farkas, Elek Attila and Wilhelm, Imola Mária and Krizbai, István Adorján and Tang, Q. and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1152/ajpheart.00709.2020},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {320},
	unique-id = {31967308},
	issn = {0363-6135},
	abstract = {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.},
	keywords = {MICROCIRCULATION; Aging; Blood-Brain Barrier; capillary density; Intravital microscopy; multiphoton microscopy},
	year = {2021},
	eissn = {1522-1539},
	pages = {H1370-H1392},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430; Kiss, Tamás/0000-0001-5339-5227; Wilhelm, Imola Mária/0000-0003-2366-7337; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:32074149,
	title = {Hypertension-induced cognitive impairment : from pathophysiology to public health},
	url = {https://m2.mtmt.hu/api/publication/32074149},
	author = {Ungvári, Zoltán István and Tóth, Péter József and Tarantini, Stefano and Prodan, Calin I and Sorond, Farzaneh and Merkely, Béla Péter and Csiszar, Anna},
	doi = {10.1038/s41581-021-00430-6},
	journal-iso = {NAT REV NEPHROL},
	journal = {NATURE REVIEWS NEPHROLOGY},
	volume = {17},
	unique-id = {32074149},
	issn = {1759-5061},
	abstract = {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.},
	year = {2021},
	eissn = {1759-507X},
	pages = {639-654},
	orcid-numbers = {Ungvári, Zoltán István/0000-0002-6035-6039; Tarantini, Stefano/0000-0001-5627-1430; Merkely, Béla Péter/0000-0001-6514-0723}
}

@article{MTMT:32558711,
	title = {Cognitive impairment in acute heart failure: Narrative review},
	url = {https://m2.mtmt.hu/api/publication/32558711},
	author = {Ventoulis, I. and Arfaras-Melainis, A. and Parissis, J. and Polyzogopoulou, E.},
	doi = {10.3390/jcdd8120184},
	journal-iso = {J CARDIOVASC DEV DIS},
	journal = {JOURNAL OF CARDIOVASCULAR DEVELOPMENT AND DISEASE},
	volume = {8},
	unique-id = {32558711},
	issn = {2308-3425},
	abstract = {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.},
	keywords = {EPIDEMIOLOGY; COGNITIVE IMPAIRMENT; acute heart failure; Neurocognitive disorder; Screening tools; Pathophysiological mechanisms; Cardiocerebral syndrome},
	year = {2021},
	eissn = {2308-3425}
}

@article{MTMT:32236169,
	title = {Application of laser speckle contrast imaging in the research on brain science},
	url = {https://m2.mtmt.hu/api/publication/32236169},
	author = {Wang, M. and Hong, J.-C. and Zhou, F.-F. and Li, P.-C.},
	doi = {10.16476/j.pibb.2021.0011},
	journal-iso = {PROG BIOCHEM BIOPHYS},
	journal = {PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS},
	volume = {48},
	unique-id = {32236169},
	issn = {1000-3282},
	abstract = {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.},
	keywords = {laser speckle contrast imaging; Hemodynamic imaging; Study of brain science},
	year = {2021},
	eissn = {1000-3282},
	pages = {922-937}
}

@article{MTMT:31623573,
	title = {Time-restricted feeding (TRF) for prevention of age-related vascular cognitive impairment and dementia},
	url = {https://m2.mtmt.hu/api/publication/31623573},
	author = {Balasubramanian, P. and DelFavero, J. and Ungvári, Anna Sára and Papp, Magor Csongor and Tarantini, A. and Price, N. and de, Cabo R. and Tarantini, Stefano},
	doi = {10.1016/j.arr.2020.101189},
	journal-iso = {AGEING RES REV},
	journal = {AGEING RESEARCH REVIEWS},
	volume = {64},
	unique-id = {31623573},
	issn = {1568-1637},
	year = {2020},
	eissn = {1872-9649},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430}
}

@article{MTMT:31624027,
	title = {The Incidence of Transverse Sinus Stenosis in Multiple Sclerosis: Further Evidence of Pulse Wave Encephalopathy},
	url = {https://m2.mtmt.hu/api/publication/31624027},
	author = {Bateman, G.A. and Lechner-Scott, J. and Bateman, A.R. and Attia, J. and Lea, R.A.},
	doi = {10.1016/j.msard.2020.102524},
	journal-iso = {MULT SCLER RELAT DIS},
	journal = {MULTIPLE SCLEROSIS AND RELATED DISORDERS},
	volume = {46},
	unique-id = {31624027},
	issn = {2211-0348},
	year = {2020},
	eissn = {2211-0356}
}

@article{MTMT:31669070,
	title = {High Cholesterol Diet Exacerbates Blood-Brain Barrier Disruption in LDLr-/- Mice: Impact on Cognitive Function},
	url = {https://m2.mtmt.hu/api/publication/31669070},
	author = {De, Oliveira J. and Engel, D.F. and De, Paula G.C. and Dos, Santos D.B. and Lopes, J.B. and Farina, M. and Moreira, E.L.G. and De, Bem A.F.},
	doi = {10.3233/JAD-200541},
	journal-iso = {J ALZHEIMERS DIS},
	journal = {JOURNAL OF ALZHEIMER'S DISEASE},
	volume = {78},
	unique-id = {31669070},
	issn = {1387-2877},
	abstract = {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.},
	keywords = {FAMILIAL HYPERCHOLESTEROLEMIA; Blood-Brain Barrier; neuroinflammation; MILD COGNITIVE IMPAIRMENT; MEMORY IMPAIRMENT; LDLr-/-mice},
	year = {2020},
	eissn = {1875-8908},
	pages = {97-115}
}

@article{MTMT:31669068,
	title = {Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography},
	url = {https://m2.mtmt.hu/api/publication/31669068},
	author = {Hill, L.K. and Hoang, D.M. and Chiriboga, L.A. and Wisniewski, T. and Sadowski, M.J. and Wadghiri, Y.Z.},
	doi = {10.3389/fnagi.2020.585218},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {12},
	unique-id = {31669068},
	issn = {1663-4365},
	abstract = {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.},
	keywords = {MRI; Blood pool agent; rarefaction; cerebral blood volume (CBV); magnetic resonance (MR) angiography; mouse brain aging},
	year = {2020},
	eissn = {1663-4365}
}

@article{MTMT:31268883,
	title = {Nicotinamide mononucleotide (NMN) supplementation promotes neurovascular rejuvenation in aged mice: transcriptional footprint of SIRT1 activation, mitochondrial protection, anti-inflammatory, and anti-apoptotic effects},
	url = {https://m2.mtmt.hu/api/publication/31268883},
	author = {Kiss, Tamás and Nyúl-Tóth, Ádám and Balasubramanian, Priya and Tarantini, Stefano and Ahire, Chetan and Yabluchanskiy, Andriy and Csípő, Tamás and Farkas, Eszter and Wren, Jonathan D. and Garman, Lori and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-020-00165-5},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {42},
	unique-id = {31268883},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {Aging; transcriptomics; Vascular cognitive impairment; Mitochondria dysfunction; geroscience},
	year = {2020},
	eissn = {2509-2723},
	pages = {527-546},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:31281265,
	title = {Single-cell RNA sequencing identifies senescent cerebromicrovascular endothelial cells in the aged mouse brain},
	url = {https://m2.mtmt.hu/api/publication/31281265},
	author = {Kiss, Tamás and Nyúl-Tóth, Ádám and Balasubramanian, Priya and Tarantini, Stefano and Ahire, Chetan and DelFavero, Jordan and Yabluchanskiy, Andriy and Csípő, Tamás and Farkas, Eszter and Wiley, Graham and Garman, Lori and Csiszar, Anna and Ungvári, Zoltán István},
	doi = {10.1007/s11357-020-00177-1},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {42},
	unique-id = {31281265},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {ALZHEIMERS-DISEASE; Aging; Blood-Brain Barrier; COGNITIVE IMPAIRMENT; senescence; NEUROVASCULAR DYSFUNCTION; SECRETORY PHENOTYPE; INDUCED CEREBRAL MICROHEMORRHAGES; AUTOREGULATORY DYSFUNCTION; IMPAIRS ANGIOGENIC CAPACITY; geroscience; VASCULAR CLEARANCE; BARRIER BREAKDOWN},
	year = {2020},
	eissn = {2509-2723},
	pages = {429-444},
	orcid-numbers = {Kiss, Tamás/0000-0001-5339-5227; Tarantini, Stefano/0000-0001-5627-1430; Farkas, Eszter/0000-0002-8478-9664; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:31349701,
	title = {Chronic imaging of mitochondria in the murine cerebral vasculature using in vivo two-photon microscopy},
	url = {https://m2.mtmt.hu/api/publication/31349701},
	author = {Rutkai, I. and Evans, W.R. and Bess, N. and Salter-Cid, T. and Cikic, S. and Chandra, P.K. and Katakam, P.V.G. and Mostany, R. and Busija, D.W.},
	doi = {10.1152/ajpheart.00751.2019},
	journal-iso = {AM J PHYSIOL HEART C},
	journal = {AMERICAN JOURNAL OF PHYSIOLOGY: HEART AND CIRCULATORY PHYSIOLOGY},
	volume = {318},
	unique-id = {31349701},
	issn = {0363-6135},
	year = {2020},
	eissn = {1522-1539},
	pages = {H1379-H1386}
}

@article{MTMT:31818613,
	title = {Does Diet Have a Role in the Treatment of Alzheimer's Disease?},
	url = {https://m2.mtmt.hu/api/publication/31818613},
	author = {Thelen, M. and Brown-Borg, H.M.},
	doi = {10.3389/fnagi.2020.617071},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {12},
	unique-id = {31818613},
	issn = {1663-4365},
	year = {2020},
	eissn = {1663-4365}
}

@article{MTMT:31400542,
	title = {Memory and Learning Deficits Are Associated With Ca2+ Dyshomeostasis in Normal Aging},
	url = {https://m2.mtmt.hu/api/publication/31400542},
	author = {Uryash, A. and Flores, V. and Adams, J.A. and Allen, P.D. and Lopez, J.R.},
	doi = {10.3389/fnagi.2020.00224},
	journal-iso = {FRONT AGING NEUROSCI},
	journal = {FRONTIERS IN AGING NEUROSCIENCE},
	volume = {12},
	unique-id = {31400542},
	issn = {1663-4365},
	year = {2020},
	eissn = {1663-4365}
}

@article{MTMT:31450313,
	title = {Increase in blood-brain barrier leakage in healthy, older adults},
	url = {https://m2.mtmt.hu/api/publication/31450313},
	author = {Verheggen, Inge C. M. and de Jong, Joost J. A. and van Boxtel, Martin P. J. and Gronenschild, Ed H. B. M. and Palm, Walter M. and Postma, Alida A. and Jansen, Jacobus F. A. and Verhey, Frans R. J. and Backes, Walter H.},
	doi = {10.1007/s11357-020-00211-2},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	volume = {42},
	unique-id = {31450313},
	issn = {2509-2715},
	abstract = {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.},
	keywords = {Permeability; Blood-Brain Barrier; Dynamic contrast-enhanced MRI; normal aging},
	year = {2020},
	eissn = {2509-2723},
	pages = {1183-1193}
}

@article{MTMT:31624028,
	title = {Blood–Brain Barrier Dysfunction in Mild Traumatic Brain Injury: Evidence From Preclinical Murine Models},
	url = {https://m2.mtmt.hu/api/publication/31624028},
	author = {Wu, Y. and Wu, H. and Guo, X. and Pluimer, B. and Zhao, Z.},
	doi = {10.3389/fphys.2020.01030},
	journal-iso = {FRONT PHYSIOL},
	journal = {FRONTIERS IN PHYSIOLOGY},
	volume = {11},
	unique-id = {31624028},
	year = {2020},
	eissn = {1664-042X}
}

@article{MTMT:31795478,
	title = {Cerebrovascular Rejuvenation: Novel Strategies for Prevention of Vascular Cognitive Impairment},
	url = {https://m2.mtmt.hu/api/publication/31795478},
	author = {Yabluchanskiy, A. and Balasubramanian, P. and Tarantini, Stefano},
	doi = {10.1089/rej.2020.2402},
	journal-iso = {REJUV RES},
	journal = {REJUVENATION RESEARCH},
	volume = {23},
	unique-id = {31795478},
	issn = {1549-1684},
	year = {2020},
	eissn = {1557-8577},
	pages = {451-452},
	orcid-numbers = {Tarantini, Stefano/0000-0001-5627-1430}
}

@article{MTMT:31692956,
	title = {Burns Impair Blood-Brain Barrier and Mesenchymal Stem Cells Can Reverse the Process in Mice},
	url = {https://m2.mtmt.hu/api/publication/31692956},
	author = {Yang, Jie and Ma, Kui and Zhang, Cuiping and Liu, Yufan and Liang, Feng and Hu, Wenzhi and Bian, Xiaowei and Yang, Siming and Fu, Xiaobing},
	doi = {10.3389/fimmu.2020.578879},
	journal-iso = {FRONT IMMUNOL},
	journal = {FRONTIERS IN IMMUNOLOGY},
	volume = {11},
	unique-id = {31692956},
	issn = {1664-3224},
	abstract = {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.},
	keywords = {Burns; Interleukin-1β; Interleukin-6; Mesenchymal Stem Cells; Brain barrier; Mfsd2a; blood–},
	year = {2020},
	eissn = {1664-3224}
}