Beta-amyloid peptide increases choline conductance of PC12 cells, which may explain the reduced level of acetylcholine in postmortem brain tissue of Alzheimer's disease patients. The increase in choline leakage out of cholinergic neurons would deplete them of the substrate for acetylcholine synthesis. Beta-amyloid also increases the activity of endogenous channels, most likely poorly selective chloride channels. Although we did not detect any changes caused by beta-amyloid in the calcium conductance an increased calcium-uptake was measured. This increase was sufficient to explain the toxic effect of peptide in culture conditions. The infusion of beta-amyloid into rat brain ventricle revealed a small increase in palmitate uptake, which implicates some membrane remodeling.
