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Mirosław Jabłoński

Researcher at Medical University of Lublin

Publications -  78
Citations -  1245

Mirosław Jabłoński is an academic researcher from Medical University of Lublin. The author has contributed to research in topics: Brain ischemia & Neurodegeneration. The author has an hindex of 18, co-authored 72 publications receiving 1061 citations. Previous affiliations of Mirosław Jabłoński include Polish Academy of Sciences.

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Alzheimer's Mechanisms in Ischemic Brain Degeneration

TL;DR: This review investigates the relationships between β‐amyloid peptide, apolipoproteins, presenilins, tau protein, α‐synuclein, inflammation factors, and neuronal survival/death decisions in brain following ischemic episode.
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Brain ischemia activates β- and γ-secretase cleavage of amyloid precursor protein: significance in sporadic Alzheimer's disease.

TL;DR: The role of brain ischemia is demonstrated as a molecular link between the β- and the γ-secretase activities and provided a molecular explanation of the possible neuropathogenesis of sporadic Alzheimer’s disease.
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Sporadic Alzheimer’s Disease Begins as Episodes of Brain Ischemia and Ischemically Dysregulated Alzheimer’s Disease Genes

TL;DR: This review attempts to depict what the authors know and do not know about the triggering factor of the Alzheimer’s disease, focusing on the possibility that the initial pathological trigger involves ischemic episodes and ischemia-induced gene dysregulation.
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Transient brain ischemia due to cardiac arrest causes irreversible long-lasting cognitive injury

TL;DR: The long-term behavioral consequences of above manipulation producing global brain ischemia were assessed in young, middle-aged and old rats, i.e., 3, 6- and 18-months post-treatment, respectively.
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Cellular markers of neuroinflammation and neurogenesis after ischemic brain injury in the long-term survival rat model

TL;DR: A balance of degenerative processes and inflammatory surveillance with neurogenesis could determine the long-term outcome of global ischemia survival or the previously proposed formation of amyloid plaques and Alzheimer’s-type dementia.