The SAMP8 mouse: a model of Alzheimer disease?
The SAMP8 mice develops early abnormalities in learning and memory. These are related to abnormalities in septohippocampal function with a decrease in serotonin leading to an increase in GABA and a decrease in acetylcholine. The cognitive defects in these animals are due to overproduction of beta-amyloid and can be reversed by antibodies to beta-amyloid or specific antisense oligonucleotides. The major defect produced by beta-amyloid in these mice appears to be reduction in delta9 desaturase activity leading to altered membrane phospholipid content. The SAMP8 mouse appears to be an excellent model to examine the pathophysiology of early defects seen in Alzheimer disease.
Morley
John E
JE
Division of Geriatric Medicine, Saint Louis University, Missouri, USA. morley@slu.edu
D000544:Alzheimer Disease / Q000503:physiopathology*; D016229:Amyloid beta-Peptides / Q000502:physiology; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D012739:Gonadal Steroid Hormones / Q000502:physiology; D006801:Humans; D008297:Male; D008568:Memory / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D018377:Neurotransmitter Agents / Q000502:physiology
D016229:Amyloid beta-Peptides; D012739:Gonadal Steroid Hormones; D018377:Neurotransmitter Agents