By Danielle Houghton
UF Professor of Neuroscience, Wolfgang J. Streit, Ph.D., further investigates the role of microglia in sporadic Alzheimer’s disease.
Microglia, which play a vital role in the brain’s immune system, have been portrayed as potentially dangerous immune effector cells. These microglia are thought to be overactivated by amyloid and, thus, producing neurotoxic inflammatory mediators that lead to neurofibrillary degeneration. Streit’s research review offers an alternative theory: the microglial dysfunction theory, “stating that microglia become impaired in their normally neuroprotective roles because of aging, i.e., they become senescent and aging neurons degenerate because they lack the needed microglial support for their survival,” according to the research.
Streit says, “The research re-introduces a novel hypothesis (microglial dysfunction) regarding the role of microglial cells in the pathogenesis of sporadic AD.” Streit first proposed and published the microglial dysfunction hypothesis in 2004 and has, since then, gathered additional human evidence in support, which is reviewed in the current publication.”
The microglial dysfunction theory incorporates aging as a critical etiological factor, noting that aging is the greatest risk factor for the sporadic (late-onset) and most common form of Alzheimer’s disease. In this review, human evidence supports senescent microglial dysfunction and conflicts with the amyloid/neuroinflammation idea. Overall, this research notably refutes the widely held view that neurodegeneration in AD is the results of chronic neuroinflammation.
Streit, who specializes in microglial biology, adds that an important takeaway from this review is “that AD cannot be treated or prevented effectively using anti-inflammatory drugs, such as aspirin or ibuprofen, or similar compounds.”