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文献和实验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
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
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