By Danielle Houghton
Professor in the Department of Neuroscience and Genetics and Genomics Program and Evelyn F. McKnight Chair for Research on Cognitive Aging and Memory, Thomas Foster, Ph. D., drives research on partial microglial depletion. Findings reveal that this depletion is associated with impaired hippocampal synaptic and cognitive function in young and aged rats.
Foster explains that microglia are the immune cells of the brain. “They protect and support neurons, but just like the periphery, excess activation may cause damage and disruption of neural circuits. Brain aging and cognitive impairment is associated with increased microglial activation (i.e. increased brain inflammation). Thus, the cognitive impairment may be due to chronic inflammation and the substances secreted by inflamed microglia).”
Foster and team, therefore, looked at what would happen if they began to decrease the number of microglia and then replenished the system with new microglia. The results indicated that cognitive function and synaptic transmission benefit from the support of aged microglia and are hindered by removal of these cells. In other words, replenishment of microglia did not better the age‐related cognitive impairments or senescent synaptic function.
“The problem is not the microglia per se, rather the conditions that activate microglia should be addressed,” says Foster. Activation may be due to aging of other cells, including cells in the periphery, which send out distress signals either locally or through the blood.
Acute activation of the immune system is a means of protecting the brain and body form bacteria, viruses, and toxins, explains Foster. However, chronic inflammation can arise due to aging and chronic diseases. Chronic activation of the immune system can have deleterious effects on brain function. Overall, the balance between acute and chronic activation of the immune system is disrupted by aging.
Foster specializes in factors that predict and contribute to age-related cognitive decline.