Fibroblasts and lymphocytes from Alzheimer patients are resistant to beta-amyloid-induced increase in the intracellular calcium concentration.

A major neuropathological finding in Alzheimer's disease (AD) is the presence of senile plaques in certain regions in the brain. The plaques contain extracellular deposits of beta-amyloid peptide (beta AP). Destabilization of intracellular calcium homeostasis in neurons, caused by beta AP, plays a central role in AD pathogenesis. In the present study, the authors report ionic alterations of lymphocytes and fibroblasts harvested from sporadic AD patients and from age-matched controls. Intracellular free calcium level ([Ca2+]i) of human cells, labeled with Fura-2AM, was determined by dual wavelength spectrofluorimetry. Basal [Ca2+]i appeared to be higher in AD lymphocytes when compared to control ones. Resting [Ca2+]i of AD fibroblasts, however, has proven to be lower than that seen with control cells. Exposure of cells to beta AP resulted in the elevation of the [Ca2+]i in both control cell types, however, that of AD lymphocytes and fibroblasts did not differ considerably.