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文献和实验Interaction of the Presenilins with the Amyloid Precursor Protein (APP)
the deposition of amyloid Aβ peptide. The latter is released from its cognate amyloid precursor protein (APP) by a two-step proteolytic conversion: first, proteolysis of APP by β-secretase, which releases the N-terminus of Aβ, and second, conversion
α-Synuclein/Amyloid Interactions
Human α-synuclein was originally identified as the precursor of a peptide named non-Aβ component of Alzheimer’s disease (NAC) that was tightly associated to purified Alzheimer’s disease amyloid (1 ). Senile amyloid plaques consist predominantly
Aβ-Induced Proinflammatory Cytokine Release from Differentiated Human THP-1 Monocytes
As noted in the introductory chapters of this book, neuritic plaques composed of accumulated amyloid β (Aβ) peptide are a hallmark pathological feature of the Alzheimer’s disease (AD) brain. Compelling genetic data now implicate these plaques
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