The pathogenic aβ43 is enriched in familial and sporadic Alzheimer disease
The amyloid-cascade hypothesis posits that the role of amyloid β-peptide (Aβ) in Alzheimer disease (AD) involves polymerization into structures that eventually are deposited as amyloid plaques. During this process, neurotoxic oligomers are formed that induce synaptic loss and neuronal death. Several...
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Veröffentlicht in: | PloS one 2013, Vol.8 (2), p.e55847 |
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Sprache: | eng |
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