@{MTMT:34823697,
	title = {Az agyi neurobiomarkerek diagnosztikus és prognosztikus értéke},
	url = {https://m2.mtmt.hu/api/publication/34823697},
	author = {Czeiter, Endre and Amrein, Krisztina},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823697},
	year = {2024},
	pages = {63-66},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944}
}

@{MTMT:34823375,
	title = {Az agysérülés neuroanatómiája},
	url = {https://m2.mtmt.hu/api/publication/34823375},
	author = {Czeiter, Endre and Fazekas, Bálint and Amrein, Krisztina},
	booktitle = {Súlyos baleseti agysérültek ellátása},
	unique-id = {34823375},
	year = {2024},
	pages = {33-46},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944; Fazekas, Bálint/0000-0002-8445-4100}
}

@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)},
	volume = {in press},
	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}
}

@article{MTMT:34477399,
	title = {Screening Performance of S100B, GFAP and UCH-L1 For Intracranial Injury Within 6 hours of Injury and beyond},
	url = {https://m2.mtmt.hu/api/publication/34477399},
	author = {Trivedi, Dhanisha Trivedi and Forssten, Maximilian Peter and Cao, Yang and Mohammad Ismail, Ahmad and Czeiter, Endre and Amrein, Krisztina and Kobeissy, Firas and Wang, Kevin K W and DeSoucy, Erik and Büki, András and Mohseni, Shahin},
	doi = {10.1089/neu.2023.0322},
	journal-iso = {J NEUROTRAUM},
	journal = {JOURNAL OF NEUROTRAUMA},
	volume = {41},
	unique-id = {34477399},
	issn = {0897-7151},
	abstract = {The Scandinavian NeuroTrauma Committee (SNC) guidelines recommend S100B as a screening tool for early detection of Traumatic brain injury (TBI) in patients presenting with an initial Glasgow coma scale (GCS) of 14-15. The objective of the current study was to compare S100B's diagnostic performance within the recommended 6-hour window after injury, compared to GFAP and UCH-L1. The secondary outcome of interest was the ability of these biomarkers in detecting traumatic intracranial pathology beyond the 6-hour mark.The Center-TBI core database (2014-2017) was queried for data pertaining to all TBI patients with an initial GCS of 14-15 who had a blood sample taken within 6 hours of injury in which the levels of S100B, GFAP, and UCH-L1 were measured. As a subgroup analysis, data involving patients with blood samples taken within 6-9 hours, and 9-12 hours were analyzed separately for diagnostic ability. The diagnostic ability of these biomarkers for detecting any intracranial injury was evaluated based on the area under the receiver operating characteristic curve (AUC). Each biomarker's sensitivity, specificity, and accuracy were also reported at the cutoff that maximized Youden's index.A total of 531 TBI patients with GCS 14-15 on admission had a blood sample taken within 6 hours, of whom 24.9% (N = 132) had radiologically confirmed intracranial injury. The AUCs of GFAP (0.86, 95% confidence interval (CI): 0.82-0.90) and UCH-L1 (0.81, 95% CI: 0.76-0.85) were statistically significantly higher than that of S100B (0.74, 95% CI: 0.69-0.79) during this time. There was no statistically significant difference in the predictive ability of S100B when sampled within 6 hours, 6-9 hours, and 9-12 hours of injury, as the p-values were >0.05 when comparing the AUCs. Overlapping AUC 95% CI suggests no benefit of a combined GFAP and UCH-L1 screening tool over GFAP during the time periods studied [ 0.87 (0.83-0.90) vs 0.86 (0.82-0.90) when sampled within 6 hours of injury, 0.83 (0.78-0.88) vs 0.83 (0.78-0.89) within 6-to-9 hours and 0.81 (0.73-0.88) vs 0.79 (0.72-0.87) within 9-12 hours].Targeted analysis of the CENTER-TBI core database, with focus on the patient category for which biomarker testing is recommended by the SNC guidelines, revealed that GFAP and UCH-L1 perform superior to S100B in predicting CT-positive intracranial lesions within 6 hours of injury. GFAP continued to exhibit superior predictive ability to S100B during the time periods studied. S100B displayed relatively unaltered screening performance beyond the diagnostic timeline provided by SNC guidelines. These findings suggest the need for a re-evaluation of the current SNC TBI guidelines.},
	keywords = {Biomarkers; traumatic brain injury; Head trauma; adult brain injury},
	year = {2024},
	eissn = {1557-9042},
	pages = {349-358},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944}
}

@article{MTMT:34474356,
	title = {Blood biomarkers for traumatic brain injury: A narrative review of current evidence},
	url = {https://m2.mtmt.hu/api/publication/34474356},
	author = {Hossain, I. and Marklund, N. and Czeiter, Endre and Hutchinson, P. and Büki, András},
	doi = {10.1016/j.bas.2023.102735},
	journal-iso = {BRAIN SPINE},
	journal = {BRAIN AND SPINE},
	volume = {4},
	unique-id = {34474356},
	issn = {2772-5294},
	year = {2024},
	orcid-numbers = {Czeiter, Endre/0000-0002-9578-6944}
}

@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: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}
}

@CONFERENCE{MTMT:33704639,
	title = {Alleviation of longterm cognitive impairment with memantine combined with alfa7 nicotic receptor ligand after repetitive mild traumatic brain injury in rats},
	url = {https://m2.mtmt.hu/api/publication/33704639},
	author = {Kolozsvári, Áron and Bali, Zsolt Kristóf and Bruszt, Nóra and Nagy, Lili Veronika and Fazekas, Bálint and Amrein, Krisztina and Czeiter, Endre and Büki, András and Hernádi, István},
	booktitle = {Joint Neuroscience Meeting of the Hungarian Neuroscience Society (MITT) & the Austrian Neuroscience Association (ANA)},
	unique-id = {33704639},
	year = {2023},
	pages = {136},
	orcid-numbers = {Bali, Zsolt Kristóf/0000-0003-0712-0788; Fazekas, Bálint/0000-0002-8445-4100; Czeiter, Endre/0000-0002-9578-6944; Hernádi, István/0000-0001-7882-4817}
}

@article{MTMT:33695777,
	title = {Traumatic Brain Injury Induces Microglial and Caspase3 Activation in the Retina},
	url = {https://m2.mtmt.hu/api/publication/33695777},
	author = {Kovács-Öller, Tamás and Zempléni, Renáta and Balogh, Boglárka and Szarka, Gergely and Fazekas, Bálint and Tengölics, Ádám Jonatán and Amrein, Krisztina and Czeiter, Endre and Hernádi, István and Büki, András and Völgyi, Béla},
	doi = {10.3390/ijms24054451},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33695777},
	issn = {1661-6596},
	abstract = {Traumatic brain injury (TBI) is among the main causes of sudden death after head trauma. These injuries can result in severe degeneration and neuronal cell death in the CNS, including the retina, which is a crucial part of the brain responsible for perceiving and transmitting visual information. The long-term effects of mild-repetitive TBI (rmTBI) are far less studied thus far, even though damage induced by repetitive injuries occurring in the brain is more common, especially amongst athletes. rmTBI can also have a detrimental effect on the retina and the pathophysiology of these injuries is likely to differ from severe TBI (sTBI) retinal injury. Here, we show how rmTBI and sTBI can differentially affect the retina. Our results indicate an increase in the number of activated microglial cells and Caspase3-positive cells in the retina in both traumatic models, suggesting a rise in the level of inflammation and cell death after TBI. The pattern of microglial activation appears distributed and widespread but differs amongst the various retinal layers. sTBI induced microglial activation in both the superficial and deep retinal layers. In contrast to sTBI, no significant change occurred following the repetitive mild injury in the superficial layer, only the deep layer (spanning from the inner nuclear layer to the outer plexiform layer) shows microglial activation. This difference suggests that alternate response mechanisms play a role in the case of the different TBI incidents. The Caspase3 activation pattern showed a uniform increase in both the superficial and deep layers of the retina. This suggests a different action in the course of the disease in sTBI and rmTBI models and points to the need for new diagnostic procedures. Our present results suggest that the retina might serve as such a model of head injuries since the retinal tissue reacts to both forms of TBI and is the most accessible part of the human brain.},
	keywords = {Brain; APOPTOSIS; INJURY; DEGENERATION; microglia; Retina; caspase; TBI},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Kovács-Öller, Tamás/0000-0002-3353-4485; Balogh, Boglárka/0000-0002-4022-8953; Fazekas, Bálint/0000-0002-8445-4100; Czeiter, Endre/0000-0002-9578-6944; Hernádi, István/0000-0001-7882-4817; Völgyi, Béla/0000-0001-7481-390X}
}

@article{MTMT:33695775,
	title = {Current Practice in Pediatric Cow's Milk Protein Allergy-Immunological Features and Beyond.},
	url = {https://m2.mtmt.hu/api/publication/33695775},
	author = {Emmert, Vanessza and Lendvai-Emmert, Dominika and Eklicsné Lepenye, Katalin and Prémusz, Viktória and Tóth, Gergely Péter},
	doi = {10.3390/ijms24055025},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {24},
	unique-id = {33695775},
	issn = {1661-6596},
	abstract = {Cow's milk protein allergy is one of the most common pediatric food allergies. It poses a significant socioeconomic burden in industrialized countries and has a profound effect on the quality of life of affected individuals and their families. Diverse immunologic pathways can lead to the clinical symptoms of cow's milk protein allergy; some of the pathomechanisms are known in detail, but others need further elucidation. A comprehensive understanding of the development of food allergies and the features of oral tolerance could have the potential to unlock more precise diagnostic tools and novel therapeutic approaches for patients with cow's milk protein allergy.},
	keywords = {epitope; immunotherapy; food allergy; cow's milk protein allergy; IgE-mediated; non-IgE-mediated},
	year = {2023},
	eissn = {1422-0067},
	orcid-numbers = {Prémusz, Viktória/0000-0002-4059-104X}
}