Article ID Journal Published Year Pages File Type
2489692 Medical Hypotheses 2011 4 Pages PDF
Abstract

Alzheimer’s disease (AD) is an age-related neurodegenerative disease. The amyloid-β (Aβ) peptide is considered a major etiological factor in the development of AD. BACE1-deficient mice and forebrain-specific conditional presenilin1 and presenilin2 double knockout mice (presenilins cDKO mice) both lack Aβ, but exhibit completely different phenotypes. The peptide p3 may play a neuroprotective role. A lack of peptide p3 could trigger an inflammatory response in the brain of presenilins cDKO mice.

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