β-Amyloid precursor protein mismetabolism and loss of calcium homeostasis in Alzheimer's disease

S. W. Barger, V. L. Smith-Swintosky, R. E. Rydel, M. P. Mattson

Research output: Contribution to journalArticlepeer-review

Abstract

The suspected involvement of the,B-amyloid precursor protein (βAPP) in the etiology of Alzheimer's disease (AD) has been strengthened by recent genetic evidence, but pursuit of the mechanisms involved will initially require basic cell biology approaches. Several studies have concentrated on toxic activities of β-amyloid peptide (βAP) itself, illuminating its contributions to excitotoxicity and calcium-mediated degeneration in general We now know that generation of βAP from βAPP also compromises the production of an important set of trophic factors: the secreted forms of βAPP (APP(S)), which may act - ironically - by conferring protection from calcium-mediated insults. Therefore, conditions which contribute to the formation of βAP (possibly including ischemia) not only produce an agent which exacerbates calcium-mediated cell death, but also reduce the levels of one of the few factors able to rescue calcium homeostasis. The implications of these postulates and their relationship to the process of aging are discussed.

Original languageEnglish (US)
Pages (from-to)158-164
Number of pages7
JournalAnnals of the New York Academy of Sciences
Volume695
DOIs
StatePublished - 1993
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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