The beta-amyloid peptide (beta A4) is a principal constituent of senil
e plagues and is thought to play a major role in the pathophysiology o
f Alzheimer's disease (AD). Although the mechanism of beta-A4 neurotox
icity is still a matter of debate, one of its effects might be a desta
bilization of cellular calcium homeostasis, thus promoting neuronal da
mage. The influence of the toxic fragment beta A25-35 on the mitogen-i
nduced rise in the intracellular calcium concentration ([Ca2+](i)) in
lymphocytes of AD (n=13) and depressive patients (n=14) as well as in
healthy controls was therefore investigated (n=16), The results showed
a significant increase in the mitogen-induced calcium signal with lym
phocytes of healthy controls and depressive patients. This beta A25-35
-induced amplification was significantly lower in AD patients as compa
red to healthy controls but not as compared to depressive patients. Th
e results thus confirm a postulated decreased beta-amyloid sensitivity
in AD lymphocytes. However, this effect might not be as pronounced or
as specific as recently decribed by Eckert et al., (1993b).