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 β-amyloid peptide (βAP). Destabilization of intracellular calcium homeostasis in neurons, caused by βAP, 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 βAP resulted in the elevation of the [Ca2+]i in both control cell types, however, that of AD lymphocytes and fibroblasts did not differ considerably.
|Number of pages||4|
|Journal||Progress in Neuro-Psychopharmacology and Biological Psychiatry|
|Publication status||Published - Jun 2002|
- Alzheimer's disease
ASJC Scopus subject areas
- Biological Psychiatry