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.
| Original language | English |
|---|---|
| Pages (from-to) | 543-546 |
| Number of pages | 4 |
| Journal | Medical Hypotheses |
| Volume | 76 |
| Issue number | 4 |
| DOIs | |
| State | Published - Apr 2011 |