Rodent exercise also slows or halts aging-related declines in the animals’ brains, studies show, in part by strengthening specialized cells called microglia. Little understood until recently, microglial cells are now known to be the brain’s resident immune cells and hall monitors. They watch for signs of waning neuronal health and, when cells in decline are spotted, release neurochemicals that initiate an inflammatory response. Inflammation, in the short-term, helps to clear away the problem cells and any other biological debris. Afterward, the microglia release other chemical messages that calm the inflammation, keeping the brain healthy and tidy and the animal’s thinking intact.
But as animals age, recent studies have found, their microglia can start to malfunction, initiating inflammation but not subsequently quieting it, leading to continuous brain inflammation. This chronic inflammation can kill healthy cells and cause problems with memory and learning, sometimes severe enough to induce a rodent version of Alzheimer’s disease.
Unless the animals exercise. In that case, post-mortem exams of their tissues show, the animals’ brains typically teem with healthy, helpful microglia deep into old age, displaying few signs of continuous brain inflammation, while the elderly rodents themselves retained a youthful ability to learn and remember.
We are not mice, though, and while we have microglia, scientists had not previously found a way to study whether being physically active as we age — or not — would influence the inner workings of microglial cells. So, for the new study, which was published in November in the Journal of Neuroscience, scientists affiliated with Rush University Medical Center in Chicago, the University of California, San Francisco, and other institutions, turned to data from the ambitious Rush Memory and Aging Project. For that study, hundreds of Chicagoans, most in their 80s at the start, completed extensive annual thinking and memory tests and wore activity monitors for at least a week. Few formally exercised, the monitors showed, but some moved around or walked far more often than others.
Many of the participants died as the study continued, and the researchers examined stored brain tissues from 167 of them, searching for lingering biochemical markers of microglial activity. They wanted to see, in effect, whether people’s microglia appeared to have been perpetually overexcited during their final years, driving brain inflammation, or been able to dial back their activity when appropriate, blunting inflammation. The researchers also looked for common biological hallmarks of Alzheimer’s disease, like the telltale plaques and tangles that riddle the brain. Then they crosschecked this data with information from people’s activity trackers.
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