Studies of the effects of fragment (25-35) of beta-amyloid peptide on the behavior of rats in a radial maze

Abstract

Decreases in cognitive functions, particularly long-term (episodic) and working memory, are among the earliest prognostic signs of Alzheimer's disease. The toxicity of beta-amyloid peptide is regarded as a major cause of neurodegeneration and cognitive impairment in this disease. The present report describes studies of the effects of intracerebroventricular administration of beta-amyloid peptide (25-35) (Abeta(25-35)) on the reproduction of a previously assimilated habit consisting of finding food in an eight-arm radial maze in rats. Abeta(25-35) was given bilaterally at doses of 15 and 30 nmol/animal seven days after preliminary training. Testing was performed 60 days after peptide administration. The results showed that Abeta(25-35) impaired working memory in rats without having any significant effect on the retention of responses. We were unable to demonstrate any relationship between memory impairment and the dose of peptide given. These data provide evidence of the ability of Abeta(25-35) to produce greater degradation of working memory function than long-term memory function.