Volume 101, Issue s121

Alzheimer's disease (AD) is a chronic condition in which inflammation has been shown to contribute to neurodegeneration. Current thinking suggests that deposition of beta-amyloid in the brain promotes inflammation resulting in neuronal damage/death. Alternatively, our data suggest that chronic inflammation observed in late-onset sporadic AD may be stimulated by infection with the obligate, intracellular bacterium, Chlamydia pneumoniae. Our results indicate that C. pneumoniae is found in high frequency in glial cells in areas of neuropathology within the brains of patients with AD. Based on our evidence, nervous system infection with C. pneumoniae should be considered a risk factor for sporadic AD.

Recent results from the author's efforts and others have indicated approaches that may eventually lead to new therapeutic strategies for combating neurodegenerative effects associated with dementia and Alzheimer's disease (AD). These strategies include unraveling mechanisms that decrease senile plaque accumulation and delay or slow the neurodegenerative progression associated with AD. Recent work addresses whether normally functioning inhibitory brain circuitry can protect and detour neurodegeneration. The aim of these research efforts is that one or a combination of these approaches will develop into an applied therapy that will enhance brain protection mechanisms and add to quality of life for patients with AD.

There is increasing evidence that free radical-induced oxidative damage may play a role in the pathogenesis of Alzheimer's disease. Free radicals are reactive oxygen compounds that may attack and damage lipids, proteins, and DNA. The brain is especially sensitive to oxidative damage because of its high content of readily oxidized fatty acids, high use of oxygen, and low levels of antioxidants. Evidence for oxidative damage has been obtained from postmortem brain tissue as well as from living patients with Alzheimer's disease. Antioxidants such as vitamin E show promise that they may help in treating the disease.