Alzheimer disease (AD) is an age-related form of dementia, the cause of which is still unknown. Abnormally high neuronal cell death is an established pathological characteristic of the disease and is especially seen in the hippocampus. It has been hypothesized that the determination of the mechansim of cell death, e.g., necrosis, apoptosis, or other forms of programmed cell death, will help elucidate the etiology of the disease. Additionally, it has been shown that b-amyloid, another pathological hallmark of AD, can induce apoptosis in cultured neurons.

We used the in situ staining terminal transferase-mediated dUTP-digoxygenin/biotin nick end labeling (TUNEL) which permits visualizing a cell's chromatin to determine the presence of apoptosis. We examined the hippocampus from autopic AD and control brain tissue and demonstrated a marked increase in apoptosis in AD tissue. In addition, using brain biopsy samples, we determined that the postmortem interval is not a factor in the quantitation. Our results suggest that programmed cell death plays a role in developing AD.

Currently, we are examining the expression of c-fos and c-jun, gene products known to be associated with apoptosis, in the above-described tissue samples.