Amyloid-β breaks brain's neuroprotection
نویسندگان
چکیده
منابع مشابه
Amyloid-β breaks brain's neuroprotection
Alzheimer’s disease (AD) is the major cause of dementia in elderly population. Neuropathological features of AD are the extracellular plaques and intracellular neurofibrillary tangles (NFTs). Plaques are composed of amyloid-β (Aβ) peptide and NFTs contain hyperphosphorylated tau protein [1]. Genetic and biochemical studies suggest that extracellular Aβ deposition triggers pathological events le...
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Amyloid-β (Aβ) deposits are seen in aged individuals of many mammalian species that possess the same aminoacid sequence as humans. This study describes Aβ deposition in 102 clinically characterized cattle brains from animals aged 0 to 20 years. Extracellular and intracellular Aβ deposition was detected with 4G8 antibody in the cortex, hippocampus, and cerebellum. X-34 staining failed to stain A...
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We report that neuronal overexpression of the endogenous inhibitor of calpains, calpastatin (CAST), in a mouse model of human Alzheimer's disease (AD) β-amyloidosis, the APP23 mouse, reduces β-amyloid (Aβ) pathology and Aβ levels when comparing aged, double transgenic (tg) APP23/CAST with APP23 mice. Concurrent with Aβ plaque deposition, aged APP23/CAST mice show a decrease in the steady-state ...
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Neuronal DNA damage may contribute to cognitive aging and the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease1,2. Aging, the main risk factor for these disorders, is associated with a progressive increase in markers of DNA breaks in neurons3. One such marker is phosphorylation of the histone protein H2A variant X at Ser139 (resulting in H2A.X), focal accumulations of whi...
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ژورنال
عنوان ژورنال: Oncotarget
سال: 2017
ISSN: 1949-2553
DOI: 10.18632/oncotarget.18246