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- W2085706266 abstract "During the last years it has become evident that the β-amyloid (Aβ) component of senile plaques may be the key molecule in the pathology of Alzheimer's disease (AD). The source and place of the neurotoxic action of Aβ, however, is still a matter of controversy. The precursor of the β-amyloid peptide is the predominantly neuronal β-amyloid precursor protein. We, and others, hypothesize that intraneuronal misregulation of APP leads to an accumulation of Aβ peptides in intracellular compartments. This accumulation impairs APP trafficking, which starts a cascade of pathological changes and causes the pyramidal neurons to degenerate. Enhanced Aβ secretion as a function of stressed neurons and remnants of degenerated neurons provide seeds for extracellular Aβ aggregates, which induce secondary degenerative events involving neighboring cells such as neurons, astroglia and macrophages/microglia." @default.
- W2085706266 created "2016-06-24" @default.
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- W2085706266 creator A5065043368 @default.
- W2085706266 date "2006-04-05" @default.
- W2085706266 modified "2023-10-18" @default.
- W2085706266 title "Key Factors in Alzheimer's Disease: β-amyloid Precursor Protein Processing, Metabolism and Intraneuronal Transport" @default.
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- W2085706266 doi "https://doi.org/10.1111/j.1750-3639.2001.tb00376.x" @default.
- W2085706266 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8098450" @default.