NDLI: Metabolism of amyloid β peptide and pathogenesis of Alzheimer's disease.

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Metabolism of amyloid β peptide and pathogenesis of Alzheimer's disease.

Content Provider	Europe PMC
Author	SAIDO, Takaomi C.
Editor	SUZUKI, Kunihiko
Copyright Year	2013
Abstract	The conversion of what has been interpreted as “normal brain aging” to Alzheimer’s disease (AD) via transition states, i.e., preclinical AD and mild cognitive impairment, appears to be a continuous process caused primarily by aging-dependent accumulation of amyloid β peptide (Aβ) in the brain. This notion however gives us a hope that, by manipulating the Aβ levels in the brain, we may be able not only to prevent and cure the disease but also to partially control some very significant aspects of brain aging. Aβ is constantly produced from its precursor and immediately catabolized under normal conditions, whereas dysmetabolism of Aβ seems to lead to pathological deposition upon aging. We have focused our attention on elucidation of the unresolved mechanism of Aβ catabolism in the brain. In this review, I describe a new approach to prevent AD development by reducing Aβ burdens in aging brains through up-regulation of the catabolic mechanism involving neprilysin that can degrade both monomeric and oligomeric forms of Aβ. The strategy of combining presymptomatic diagnosis with preventive medicine seems to be the most pragmatic in both medical and socioeconomical terms.
Related Links	https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC3758963&blobtype=pdf
ISSN	03862208
Journal	Proceedings of the Japan Academy. Series B, Physical and Biological Sciences [Proc Jpn Acad Ser B Phys Biol Sci]
Volume Number	89
DOI	10.2183/pjab.89.321
PubMed Central reference number	PMC3758963
Issue Number	7
PubMed reference number	23883611
e-ISSN	13492896
Language	English
Publisher	The Japan Academy
Publisher Date	2013-01-01
Publisher Place	Tokyo, Japan
Access Restriction	Open
Rights License	This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Japan Academy
Subject Keyword	Alzheimer’s disease (AD) mild cognitive impairment (MCI) preclinical AD amyloid β peptide (Aβ) metabolism neprilysin secretase
Content Type	Text
Resource Type	Article
Subject	Physics and Astronomy Medicine Agricultural and Biological Sciences

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