@article{MTMT:34804161,
	title = {Atherosclerotic burden and cerebral small vessel disease : exploring the link through microvascular aging and cerebral microhemorrhages},
	url = {https://m2.mtmt.hu/api/publication/34804161},
	author = {Csiszar, Anna and Ungvári, Anna Sára and Patai, Roland and Gulej, Rafal and Yabluchanskiy, Andriy and Benyó, Zoltán and Kovács, Illés and Sótonyi, Péter and Kirkpartrick, Angelia C and Prodan, Calin I and Liotta, Eric M and Zhang, Xin A and Tóth, Péter József and Tarantini, Stefano and Sorond, Farzaneh A and Ungvári, Zoltán István},
	doi = {10.1007/s11357-024-01139-7},
	journal-iso = {GEROSCIENCE},
	journal = {GEROSCIENCE: OFFICIAL JOURNAL OF THE AMERICAN AGING ASSOCIATION (AGE)},
	unique-id = {34804161},
	issn = {2509-2715},
	abstract = {Cerebral microhemorrhages (CMHs, also known as cerebral microbleeds) are a critical but frequently underestimated aspect of cerebral small vessel disease (CSVD), bearing substantial clinical consequences. Detectable through sensitive neuroimaging techniques, CMHs reveal an extensive pathological landscape. They are prevalent in the aging population, with multiple CMHs often being observed in a given individual. CMHs are closely associated with accelerated cognitive decline and are increasingly recognized as key contributors to the pathogenesis of vascular cognitive impairment and dementia (VCID) and Alzheimer's disease (AD). This review paper delves into the hypothesis that atherosclerosis, a prevalent age-related large vessel disease, extends its pathological influence into the cerebral microcirculation, thereby contributing to the development and progression of CSVD, with a specific focus on CMHs. We explore the concept of vascular aging as a continuum, bridging macrovascular pathologies like atherosclerosis with microvascular abnormalities characteristic of CSVD. We posit that the same risk factors precipitating accelerated aging in large vessels (i.e., atherogenesis), primarily through oxidative stress and inflammatory pathways, similarly instigate accelerated microvascular aging. Accelerated microvascular aging leads to increased microvascular fragility, which in turn predisposes to the formation of CMHs. The presence of hypertension and amyloid pathology further intensifies this process. We comprehensively overview the current body of evidence supporting this interconnected vascular hypothesis. Our review includes an examination of epidemiological data, which provides insights into the prevalence and impact of CMHs in the context of atherosclerosis and CSVD. Furthermore, we explore the shared mechanisms between large vessel aging, atherogenesis, microvascular aging, and CSVD, particularly focusing on how these intertwined processes contribute to the genesis of CMHs. By highlighting the role of vascular aging in the pathophysiology of CMHs, this review seeks to enhance the understanding of CSVD and its links to systemic vascular disorders. Our aim is to provide insights that could inform future therapeutic approaches and research directions in the realm of neurovascular health.},
	keywords = {ATHEROSCLEROSIS; Aging; Blood-Brain Barrier; Arteriosclerosis; stroke; Leukoaraiosis; Peripheral artery disease; VASCULAR DEMENTIA; Microbleed; White matter hyperintensities; white matter injury},
	year = {2024},
	eissn = {2509-2723},
	orcid-numbers = {Benyó, Zoltán/0000-0001-6015-0359; Kovács, Illés/0000-0001-5763-0482; Sótonyi, Péter/0000-0002-2216-4298; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@misc{MTMT:34794821,
	title = {Neural correlates of valence and arousal ratings responding to socio-emotional stimuli.},
	url = {https://m2.mtmt.hu/api/publication/34794821},
	author = {Rendes, Réka and Orsi, Gergely and Perlaki, Gábor and Bereczkei, Tamás and Deák, Anita},
	unique-id = {34794821},
	year = {2024},
	orcid-numbers = {Bereczkei, Tamás/0000-0002-4665-3475; Deák, Anita/0000-0001-6862-4993}
}

@article{MTMT:34477401,
	title = {Impaired Neurovascular Coupling and Increased Functional Connectivity in the Frontal Cortex Predict Age-Related Cognitive Dysfunction},
	url = {https://m2.mtmt.hu/api/publication/34477401},
	author = {Mukli, Péter and Pinto, Camila B and Owens, Cameron D and Csípő, Tamás and Lipécz, Ágnes and Szarvas, Zsófia and Péterfi, Anna and Langley, Ana Clara da Costa Pinaffi and Hoffmeister, Jordan and Rácz, Frigyes Sámuel and Perry, Jonathan W and Tarantini, Stefano and Nyúl-Tóth, Ádám and Sorond, Farzaneh A and Yang, Yuan and James, Judith A and Kirkpatrick, Angelia C and Prodan, Calin I and Tóth, Péter József and Galindo, Juliette and Gardner, Andrew W and Sonntag, William E and Csiszar, Anna and Ungvári, Zoltán István and Yabluchanskiy, Andriy},
	doi = {10.1002/advs.202303516},
	journal-iso = {ADV SCI},
	journal = {ADVANCED SCIENCE},
	volume = {11},
	unique-id = {34477401},
	abstract = {Impaired cerebrovascular function contributes to the genesis of age-related cognitive decline. In this study, the hypothesis is tested that impairments in neurovascular coupling (NVC) responses and brain network function predict cognitive dysfunction in older adults. Cerebromicrovascular and working memory function of healthy young (n = 21, 33.2±7.0 years) and aged (n = 30, 75.9±6.9 years) participants are assessed. To determine NVC responses and functional connectivity (FC) during a working memory (n-back) paradigm, oxy- and deoxyhemoglobin concentration changes from the frontal cortex using functional near-infrared spectroscopy are recorded. NVC responses are significantly impaired during the 2-back task in aged participants, while the frontal networks are characterized by higher local and global connection strength, and dynamic FC (p < 0.05). Both impaired NVC and increased FC correlate with age-related decline in accuracy during the 2-back task. These findings suggest that task-related brain states in older adults require stronger functional connections to compensate for the attenuated NVC responses associated with working memory load.},
	keywords = {Aging; cognitive decline; functional connectivity; Neurovascular coupling; functional near-infrared spectroscopy},
	year = {2024},
	eissn = {2198-3844},
	orcid-numbers = {Mukli, Péter/0000-0003-4355-8103; Szarvas, Zsófia/0000-0002-0022-5053; Rácz, Frigyes Sámuel/0000-0001-9077-498X; Tarantini, Stefano/0000-0001-5627-1430; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34226087,
	title = {Structural neural correlates of mental fatigue and reward-induced improvement in performance},
	url = {https://m2.mtmt.hu/api/publication/34226087},
	author = {Matuz, András and Darnai, Gergely and Zsidó, András Norbert and Janszky, József Vladimír and Csathó, Árpád},
	doi = {10.1007/s42977-023-00187-y},
	journal-iso = {BIOL FUTURA},
	journal = {BIOLOGIA FUTURA},
	unique-id = {34226087},
	issn = {2676-8615},
	abstract = {Neuroimaging studies investigating the association between mental fatigue (henceforth fatigue) and brain physiology have identified many brain regions that may underly the cognitive changes induced by fatigue. These studies focused on the functional changes and functional connectivity of the brain relating to fatigue. The structural correlates of fatigue, however, have received little attention. To fill this gap, this study explored the associations of fatigue with cortical thickness of frontal and parietal regions. In addition, we aimed to explore the associations between reward-induced improvement in performance and neuroanatomical markers in fatigued individuals. Thirty-nine healthy volunteers performed the psychomotor vigilance task for 15 min (i.e., 3 time-on-task blocks of 5 min) out of scanner; followed by an additional rewarded block of the task lasting 5 min. Baseline high-resolution T1-weigthed MR images were obtained. Reaction time increased with time-on-task but got faster again in the rewarded block. Participants’ subjective fatigue increased during task performance. In addition, we found that higher increase in subjective mental fatigue was associated with the cortical thickness of the following areas: bilateral precuneus, right precentral gyrus; right pars triangularis and left superior frontal gyrus. Our results suggest that individual differences in subjective mental fatigue may be explained by differences in the degree of cortical thickness of areas that are associated with motor processes, executive functions, intrinsic alertness and are parts of the default mode network.},
	year = {2024},
	eissn = {2676-8607},
	orcid-numbers = {Zsidó, András Norbert/0000-0003-0506-6861; Janszky, József Vladimír/0000-0001-6100-832X}
}

@article{MTMT:34113102,
	title = {Gray Matter Changes Following Mild COVID-19 : An MR Morphometric Study in Healthy Young People},
	url = {https://m2.mtmt.hu/api/publication/34113102},
	author = {Perlaki, Gábor and Darnai, Gergely and Arató, Ákos and Alhour, Husamalddin Ali Mohammad and Szente, Anna Tímea and Áfra, Eszter and Nagy, Szilvia Anett and Horváth, Réka and Kovács, Norbert and Dóczi, Tamás Péter and Orsi, Gergely and Janszky, József Vladimír},
	doi = {10.1002/jmri.28970},
	journal-iso = {JMRI - J MAGN RESON IM},
	journal = {JOURNAL OF MAGNETIC RESONANCE IMAGING},
	unique-id = {34113102},
	issn = {1053-1807},
	abstract = {Although COVID-19 is primarily an acute respiratory infection, 5%-40% of patients develop late and prolonged symptoms with frequent neurological complaints, known as long COVID syndrome. The presentation of the disease suggests that COVID infection may cause functional and/or morphological central nervous system alterations, but studies published in the literature report contradictory findings.To investigate the chronic effects of COVID-19 on cerebral grey matter in a group of young patients without comorbidities, with mild course of COVID infection and no medical complaints at the time of examination.Prospective.Thirty-eight young (age = 26.6 ± 5.0 years; male/female = 14/24), adult participants who recovered from mild COVID infection without a history of clinical long COVID and 37 healthy control subjects (age = 25.9 ± 2.8 years; male/female = 14/23).Three Tesla, 3D T1-weighted magnetization-prepared rapid gradient-echo, 2D T2-weighted turbo spin-echo.MRI-based morphometry and volumetry along with neuropsychological testing and self-assessed questionnaire.Fisher's exact test, Mann-Whitney U-test, and multiple linear regression analyses were used to assess differences between COVID and healthy control groups. P < 0.05 was used as cutoff for significance.In the COVID group, significantly lower bilateral mean cortical thickness (left/right-hemisphere: 2.51 ± 0.06 mm vs. 2.56 ± 0.07 mm, η2 p  = 0.102/2.50 ± 0.06 mm vs. 2.54 ± 0.07 mm, η2 p  = 0.101), lower subcortical gray matter (57881 ± 3998 mm3 vs. 60470 ± 5211 mm3 , η2 p  = 0.100) and lower right olfactory bulb volume (52.28 ± 13.55 mm3 vs. 60.98 ± 15.8 mm3 , η2 p  = 0.078) were found. In patients with moderate to severe anosmia, cortical thickness was significantly lower bilaterally, as compared to patients without olfactory function loss (left/right-hemisphere: 2.50 ± 0.06 mm vs. 2.56 ± 0.05 mm, η2  = 0.173/2.49 ± 0.06 mm vs. 2.55 ± 0.05 mm, η2  = 0.189). Using further exploratory analysis, significantly reduced cortical thickness was detected locally in the right lateral orbitofrontal cortex in the COVID group (2.53 ± 0.10 mm vs. 2.60 ± 0.09 mm, η2 p  = 0.112).Even without any subjective or objective neurological complaints at the time of the MR scan, subjects in the COVID group showed gray matter alterations in cortical thickness and subcortical gray matter volume.2 TECHNICAL EFFICACY: Stage 3.},
	keywords = {Brain; morphometry; cortical thickness; SARS-CoV-2},
	year = {2024},
	eissn = {1522-2586},
	orcid-numbers = {Alhour, Husamalddin Ali Mohammad/0000-0001-5841-1652; Nagy, Szilvia Anett/0000-0001-6483-9209; Kovács, Norbert/0000-0002-7332-9240; Janszky, József Vladimír/0000-0001-6100-832X}
}

@article{MTMT:34392087,
	title = {Mild traumatic brain injury-induced persistent blood–brain barrier disruption is prevented by cyclosporine A treatment in hypertension},
	url = {https://m2.mtmt.hu/api/publication/34392087},
	author = {Lendvai-Emmert, Dominika and Magyar-Sümegi, Zsófia Dina and Hegedüs, Emőke and Szarka, Nikolett and Fazekas, Bálint and Amrein, Krisztina and Czeiter, Endre and Büki, András and Ungvári, Zoltán István and Tóth, Péter József},
	doi = {10.3389/fneur.2023.1252796},
	journal-iso = {FRONT NEUR},
	journal = {FRONTIERS IN NEUROLOGY},
	volume = {14},
	unique-id = {34392087},
	issn = {1664-2295},
	year = {2023},
	eissn = {1664-2295},
	orcid-numbers = {Fazekas, Bálint/0000-0002-8445-4100; Czeiter, Endre/0000-0002-9578-6944; Ungvári, Zoltán István/0000-0002-6035-6039}
}

@article{MTMT:34106202,
	title = {Comment on “Summing MDS-UPDRS Parts 1 + 2 (Nonmotor and Motor Experience of Daily Living): The Patient's Voice”},
	url = {https://m2.mtmt.hu/api/publication/34106202},
	author = {Kovács, Norbert and Aschermann, Zsuzsanna and Harmat, Márk and Rohonczi, Mirtill and Janszky, József Vladimír and Pintér, Dávid},
	doi = {10.1002/mds.29512},
	journal-iso = {MOVEMENT DISORD},
	journal = {MOVEMENT DISORDERS},
	volume = {38},
	unique-id = {34106202},
	issn = {0885-3185},
	year = {2023},
	eissn = {1531-8257},
	pages = {1563-1564},
	orcid-numbers = {Kovács, Norbert/0000-0002-7332-9240; Janszky, József Vladimír/0000-0001-6100-832X}
}

@article{MTMT:34050791,
	title = {Prognostic Value of Serum Biomarkers in Patients With Moderate-Severe Traumatic Brain Injury, Differentiated by Marshall Computer Tomography Classification},
	url = {https://m2.mtmt.hu/api/publication/34050791},
	author = {Richter, Sophie and Czeiter, Endre and Amrein, Krisztina and Mikolic, Ana and Verheyden, Jan and Wang, Kevin K and Maas, Andrew and Steyerberg, Ewout and Büki, András and Menon, David and Newcombe, Virginia},
	doi = {10.1089/neu.2023.0029},
	journal-iso = {J NEUROTRAUM},
	journal = {JOURNAL OF NEUROTRAUMA},
	volume = {40},
	unique-id = {34050791},
	issn = {0897-7151},
	abstract = {Prognostication is challenging in traumatic brain injury (TBI) patients in whom the CT fails to fully explain a low level of consciousness. Serum biomarkers reflect the extent of structural damage in a different way than CT does, but it is unclear if biomarkers provide additional prognostic value across the range of CT abnormalities. This study aimed to determine the added predictive value of biomarkers, differentiated by imaging severity. This prognostic study used data from the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) study (2014-2017). The analysis included patients aged ≥16 years with a moderate-severe TBI (Glasgow Coma Scale, GCS < 13) who had an acute CT and serum biomarkers obtained ≤24h of injury. Out of six protein biomarkers (GFAP, NFL, NSE, S100B, Tau, UCH-L1) the most prognostic panel was selected using lasso regression. The performance of established prognostic models (CRASH and IMPACT) was assessed before and after the addition of the biomarker panel, and compared between patients with different CT Marshall scores (Marshall score <3 versus Marshall score ≥3). Outcome was assessed at 6 months post-injury using the extended Glasgow Outcome Scale (GOSE), and dichotomized into favorable and unfavourable (GOSE <5). We included 872 patients with moderate-severe TBI. The mean age was 47 years (range 16 - 95), 647 (74%) were male and 438 (50%) had a Marshall CT score <3. The serum biomarkers GFAP, NFL, S100B and UCH-L1 provided complementary prognostic information, NSE and Tau showed no added value. The addition of the biomarker panel to established prognostic models increased the area under the curve (AUC) by 0.08 and 0.03, and the explained variation in outcome by 13-14% and 7-8%, for patients with a Marshall score of <3 and ≥3, respectively. The incremental AUC of biomarkers for individual models was significantly greater when the Marshall score was <3 compared to ≥3 (p < 0.001). Serum biomarkers improve outcome prediction after moderate-severe TBI across the range of imaging severities and especially in patients with a Marshall score <3.},
	keywords = {Biomarkers; prospective study; traumatic brain injury; adult brain injury; CT scanning},
	year = {2023},
	eissn = {1557-9042},
	pages = {2297-2310},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944}
}

@article{MTMT:34050785,
	title = {White matter hyperintensities associated with impulse control disorders in Parkinson's Disease},
	url = {https://m2.mtmt.hu/api/publication/34050785},
	author = {Hernádi, Gabriella and Perlaki, Gábor and Kovács, Márton and Pintér, Dávid and Orsi, Gergely and Janszky, József Vladimír and Kovács, Norbert},
	doi = {10.1038/s41598-023-37054-8},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {13},
	unique-id = {34050785},
	issn = {2045-2322},
	abstract = {Impulse control disorders (ICDs) in Parkinson's disease (PD) are increasingly recognized as clinically significant non-motor features that potentially impair the quality of life. White matter hyperintensities (WMHs), detected by magnetic resonance imaging, are frequently observed in PD and can be associated with both motor- and certain non-motor symptoms. Given the limited number of non-motor features studied in this context, our aim was to reveal the potential association between the severity of WMHs and ICDs in PD. Fluid-attenuated inversion recovery magnetic resonance images were retrospectively evaluated in 70 patients with PD (48 males; 59.3 ± 10.1 years). The severity of WMHs was assessed by Fazekas scores and by the volume and number of supratentorial WMHs. ICDs were evaluated using the modified Minnesota Impulsive Disorders Interview. Significant interaction between age and the severity of WMHs was present for ICDs. In our younger patients (< 60.5 years), severity of WMHs was positively associated with ICDs (p = 0.004, p = 0.021, p < 0.001 and p < 0.001, respectively for periventricular white matter and total Fazekas scores and the volume and number of WMHs). Our study supports the hypothesis that WMHs of presumed vascular origin may contribute to ICDs in PD. Future prospective studies are needed to assess the prognostic relevance of this finding.},
	year = {2023},
	eissn = {2045-2322},
	orcid-numbers = {Janszky, József Vladimír/0000-0001-6100-832X; Kovács, Norbert/0000-0002-7332-9240}
}

@misc{MTMT:34012058,
	title = {Fehérállományi hiperintenzitások és impulzus kontroll zavarok kapcsolata Parkinson-kórban},
	url = {https://m2.mtmt.hu/api/publication/34012058},
	author = {Kovács, Márton and Hernádi, Gabriella and Perlaki, Gábor and Pintér, Dávid and Orsi, Gergely and Janszky, József Vladimír and Kovács, Norbert},
	unique-id = {34012058},
	year = {2023},
	orcid-numbers = {Janszky, József Vladimír/0000-0001-6100-832X; Kovács, Norbert/0000-0002-7332-9240}
}