Reduced beta-amyloid response in lymphocytes of patients with Alzheimer's disease.
The beta-amyloid peptide (beta A4) is a principal constituent of senile plaques and is thought to play a major role in the pathophysiology of Alzheimer's disease (AD). Although the mechanism of beta-A4 neurotoxicity is still a matter of debate, one of its effects might be a destabilization of cellular calcium homeostasis, thus promoting neuronal damage. The influence of the toxic fragment beta A25-35 on the mitogen-induced 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 lymphocytes of healthy controls and depressive patients. This beta A25-35-induced amplification was significantly lower in AD patients as compared to healthy controls but not as compared to depressive patients. The 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 described by Eckert et al., (1993b).
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D003866:Depressive Disorder / Q000378:metabolism; D005260:Female; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D008875:Middle Aged
D016229:Amyloid beta-Peptides