Abstract
The senescence accelerate mouse P8 (SAMP8) is an excellent model of early learning and memory problems. A number of studies have shown that it has cholinergic deficits, oxidative damage, alterations in membrane lipids and circadian rhythm disturbances. The brains of the SAMP8 overproduce amyloid precursor protein (APP), amyloid-beta protein and have an increased physphorylation of tau. An antisense to APP has been developed that reverses the cognitive deficits and oxidative damage. This antisense represents a poten-tial treatment for Alzheimers disease.
Keywords: Antisense, amyloid-beta, SAMP8, oxidative damage, Alzheimer's, blood brain barrier, testosterone, amyloid precursor protein (APP), cognitive deficits
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