부산대학교 도서관

Immediate post-training intracerebroven-tricular administration of a synthetic peptide homologous to β protein of brain amyloid, [Gln 11 ]β-(1-28), caused amnesia for footshock active avoidance training in mice in a dose-dependent fashion. This effect was specific to memory processing since the peptide did not cause amnesia when injected 24 hr after training nor did it disturb storage or retrieval of older memories. Shorter fragments of the amyloid β protein consisting of residues 12-28, 18-28, and 12-20 also were amnestic when given intracerebroventricularly, residues 12-20 being least effective. The hippocampus, a brain structure importantly involved in learning and memory, consistently shows severe pathological changes and deposition of amyloid in patients with Alzheimer disease. Immediate post-training bilateral intrahip-pocampal injection of [Gln 11 ]β-(1-28) produced amnesia at much lower doses than did [Gln 11 ]β-(1-28) injected intracere-broventricularly. Thus these experimental results suggest a possible direct role of amyloid β protein or fragments thereof in an aspect of the spectrum of cognitive deficit in Alzheimer disease.