Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2489692 | Medical Hypotheses | 2011 | 4 Pages |
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.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Developmental Biology
Authors
Wenfei Han, Tingting Ji, Bing Mei, Jiansheng Su,