Reduced β-Amyloid Response in Lymphocytes of Patients with Alzheimer's Disease

Abstract

The β-amyloid peptide (βA4) 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 β-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 βA25-35 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 βA25-35-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 β-amyloid sensitivity in AD lymphocytes. However, this effect might not be as pronounced or as specific as recently decribed by Eckert et al., (1993b).