The beta-amyloid peptide-25-35 (beta A25-35) decreases the fluidity of
mouse brain membranes in a concentration-depending fashion. First eff
ects were already seen at a beta A25-35 concentration of 100 nmol/l. b
eta-Amyloid peptide(1-40) was similarly active. beta A25-35 also decre
ases the fluidity of human lymphocyte membranes and of membranes from
the cortex, hippocampus, striatum, and cerebellum of the rat, although
the effects in the rat cerebellum are only weak. Scrambled beta A25-3
5 when investigated under similar conditions showed no effects on memb
rane fluidity. It is suggest that the effect on cellular calcium-signa
lling but also the neurotoxic properties of beta-amyloid might be the
result of its concentration depending effects on membrane properties.