Nucleotides released from Aβ1-42-treated microglial cells increase cell migration and Aβ1-42 uptake through P2Y2 receptor activation
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Enhanced Aβ1–40 Production in Endothelial Cells Stimulated with Fibrillar Aβ1–42
Amyloid accumulation in the brain of Alzheimer's patients results from altered processing of the 39- to 43-amino acid amyloid β protein (Aβ). The mechanisms for the elevated amyloid (Aβ(1-42)) are considered to be over-expression of the amyloid precursor protein (APP), enhanced cleavage of APP to Aβ, and decreased clearance of Aβ from the central nervous system (CNS). We report herein studies o...
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ژورنال
عنوان ژورنال: Journal of Neurochemistry
سال: 2012
ISSN: 0022-3042
DOI: 10.1111/j.1471-4159.2012.07700.x