Contributed by: Michael Rafii, M.D., Ph.D - Director of the Memory Disorders Clinic at the University of California, San Diego. _______________________________
For many years, it’s been believed that brain inflammation contributes to the development of Alzheimer’s disease, and based on that claim, numerous clinical trials with anti-inflammatory drugs have been conducted. However, they have all been unsuccessful in slowing the disease.
Now, researchers with the University of Florida, in collaboration with scientists at the University of Frankfurt, Germany, have discovered a possible explanation for the lack of efficacy seen witih anti-inflammatory drugs in AD: inflammation of microglia — an abundant cell type that plays an important supporting role in the brain — does not appear to be associated with dementia in Alzheimer’s disease.
Glial cells, including microgia, outnumber neurons 10-to-1. Inflammation theories of AD suggest that microglia become “activated” and mount an immune response to beta-amyloid, and instead of being helpful, actually cause damage to neurons, worsening the disease effects.
However, the researchers used high-resolution imaging techniques to look at microglial activation in AD brains and their observations did not find evidence that Abeta activates, or inflames, human microglia cells. Nor did they find evidence that inflammation is to blame for neuronal death.
Thus, it may be that beta amyloid is causing all of the damage, and that microglial cells are simply witnesses to the incident, and not active participants.
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