GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.
Li
Yazhou
Y
Laboratory of Neurosciences, Intramural Research Program, National Institute on Aging, Baltimore, MD, USA.
Duffy
Kara B
KB
Ottinger
Mary Ann
MA
Ray
Balmiki
B
Bailey
Jason A
JA
Holloway
Harold W
HW
Tweedie
David
D
Perry
Tracyann
T
Mattson
Mark P
MP
Kapogiannis
Dimitrios
D
Sambamurti
Kumar
K
Lahiri
Debomoy K
DK
Greig
Nigel H
NH
D000544:Alzheimer Disease / Q000453:epidemiology / Q000378:metabolism* / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism* / Q000473:pathology*; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D004195:Disease Models, Animal; D005260:Female; D000067757:Glucagon-Like Peptide-1 Receptor; D051379:Mice; D008822:Mice, Transgenic; D018384:Oxidative Stress / Q000502:physiology; D018027:Receptors, Glucagon / Q000378:metabolism*; D016875:tau Proteins / Q000378:metabolism
D016229:Amyloid beta-Peptides; C000593833:GLP1R protein, human; C000593834:Glp1r protein, mouse; D000067757:Glucagon-Like Peptide-1 Receptor; D018027:Receptors, Glucagon; D016875:tau Proteins