Peptide p3 may play a neuroprotective role in the brain.
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.
School of Stomatology, Tongji University, Shanghai 200072, China.
Wenfei
W
Han
Tingting
T
Ji
Bing
B
Mei
Jiansheng
J
Su
D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000473:pathology*; D002352:Carrier Proteins / Q000235:genetics / Q000502:physiology*; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D051379:Mice; D018345:Mice, Knockout; D010455:Peptides / Q000235:genetics / Q000502:physiology*; D053764:Presenilin-1 / Q000235:genetics; D053766:Presenilin-2 / Q000235:genetics
D016564:Amyloid beta-Protein Precursor; D002352:Carrier Proteins; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D053764:Presenilin-1; D053766:Presenilin-2; C485059:peptide P3