Journal ArticleDOI
Alzheimer's Mechanisms in Ischemic Brain Degeneration
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TLDR
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.Abstract:
There is increasing evidence for influence of Alzheimer's proteins and neuropathology on ischemic brain injury. This review investigates the relationships between beta-amyloid peptide, apolipoproteins, presenilins, tau protein, alpha-synuclein, inflammation factors, and neuronal survival/death decisions in brain following ischemic episode. The interactions of these molecules and influence on beta-amyloid peptide synthesis and contribution to ischemic brain degeneration and finally to dementia are reviewed. Generation and deposition of beta-amyloid peptide and tau protein pathology are important key players involved in mechanisms in ischemic neurodegeneration as well as in Alzheimer's disease. Current evidence suggests that inflammatory process represents next component, which significantly contribute to degeneration progression. Although inflammation was initially thought to arise secondary to ischemic neurodegeneration, recent studies present that inflammatory mediators may stimulate amyloid precursor protein metabolism by upregulation of beta-secretase and therefore are able to establish a vicious cycle. Functional brain recovery after ischemic lesion was delayed and incomplete by an injury-related increase in the amount of the neurotoxic C-terminal of amyloid precursor protein and beta-amyloid peptide. Moreover, ischemic neurodegeneration is strongly accelerated with aging, too. New therapeutic alternatives targeting these proteins and repairing related neuronal changes are under development for the treatment of ischemic brain consequences including memory loss prevention.read more
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The aging brain and cognition: contribution of vascular injury and aβ to mild cognitive dysfunction
Natalie L. Marchant,Bruce R Reed,Nerses Sanossian,Cindee Madison,Stephen Kriger,Roxana Dhada,Wendy J. Mack,Charles DeCarli,Michael W. Weiner,Dan M Mungas,Helena C. Chui,William J. Jagust +11 more
TL;DR: VBI was more influential than Aβ in contemporaneous cognitive function and remained predictive after including the possible influence of Aβ, and the impact of cerebrovascular disease should be considered with respect to defining the etiology of mild cognitive impairment.
Journal ArticleDOI
Brain ischemia activates β- and γ-secretase cleavage of amyloid precursor protein: significance in sporadic Alzheimer's disease.
Ryszard Pluta,Wanda Furmaga-Jabłońska,Ryszard Maciejewski,Marzena Ułamek-Kozioł,Mirosław Jabłoński +4 more
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.
Journal ArticleDOI
Sporadic Alzheimer’s Disease Begins as Episodes of Brain Ischemia and Ischemically Dysregulated Alzheimer’s Disease Genes
Ryszard Pluta,Mirosław Jabłoński,Marzena Ułamek-Kozioł,Janusz Kocki,Judyta Brzozowska,Sławomir Januszewski,Wanda Furmaga-Jabłońska,Anna Bogucka-Kocka,Ryszard Maciejewski,Stanisław J. Czuczwar +9 more
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.
Journal ArticleDOI
Cellular markers of neuroinflammation and neurogenesis after ischemic brain injury in the long-term survival rat model
Vera Sekeljic,Danijela Bataveljic,Stefan Stamenković,Marzena Ułamek,Mirosław Jabłoński,Lidija Radenovic,Ryszard Pluta,Pavle R. Andjus +7 more
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.
Journal ArticleDOI
APP as a Protective Factor in Acute Neuronal Insults
Dimitri Hefter,Andreas Draguhn +1 more
TL;DR: The current understanding of the neuroprotective role of APP and APPsα is summarized and possible implications for future research and new therapeutic strategies are summarized.
References
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Journal ArticleDOI
Delayed neuronal death in the gerbil hippocampus following ischemia
TL;DR: These changes in CA1, called here 'delayed neuronal death', may differ from those thought to be typical of ischemic neuronal damage, and it is unlikely that the disturbance of local blood vessels was the cause of these changes.
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Temporal profile of neuronal damage in a model of transient forebrain ischemia.
TL;DR: The unique delay in onset of ischemic cell change and the protracte increase in its incidence between 24 and 72 hours could reflect either delayed‐appearance of isChemic change in previously killed neurons or a delayed insult that continued to jeopardize compromised but otherwise viable neurons during the postischemic period.
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Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
Alexei Degterev,Zhihong Huang,Michael Boyce,Yaqiao Li,Prakash Jagtap,Noboru Mizushima,Gregory D. Cuny,Timothy J. Mitchison,Michael A. Moskowitz,Junying Yuan +9 more
TL;DR: It is demonstrated that necroptosis contributes to delayed mouse ischemic brain injury in vivo through a mechanism distinct from that of apoptosis and offers a new therapeutic target for stroke with an extended window for neuroprotection.
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Reactive oxygen radicals in signaling and damage in the ischemic brain.
TL;DR: Transgenic or knockout mice with cell- or site-specific prooxidant and antioxidant enzymes provide useful tools in dissecting the events involving oxidative stress in signaling and damage in ischemic brain injury.
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Astrocyte activation and reactive gliosis
Milos Pekny,Michael Nilsson +1 more
TL;DR: Astrocytes become activated (reactive) in response to many CNS pathologies, such as stroke, trauma, growth of a tumor, or neurodegenerative disease, and its possible roles in the CNS trauma and ischemia are discussed.