An amyloid beta-protein fragment, A beta[12-28], equipotently impairs post-training memory processing when injected into different limbic system structures.

Previously, amyloid beta-protein (A beta) fragments 1-28, 12-28 and 12-20 were found to impair retention in mice when injected intracerebroventricularly after footshock active avoidance training. We now have measured the dose-dependence of amnestic effects of peptide 12-28 stereotactically injected into amygdala, caudate, hippocampus, mammillary bodies and septum, which limbic structures are known to be involved in memory processing and into the medial thalamus, which largely is involved in sensory processing during training. Peptide 12-28 impaired retention with remarkably similar efficacy when injected into limbic structures but was not at all amnestic upon thalamic injection. Present results together with those in the literature lead us to suggest that A beta may exert dysregulatory cognitive effects by incoordination of K(+)-channel function in neurons, glia and endothelial cells.