Rodent training also slows or halts aging-related decline in the animals’ brains, studies show, in part by strengthening specialized cells called microglia. Until recently it was little understood, but it is now known that microglial cells are the immune cells and hall monitors of the brain. They watch for signs of declining neuronal health, and when cells in decay are signaled, they release neurochemicals that initiate an inflammatory response. In the short term, inflammation helps to clear out the problem cells and other biological waste. Then the microglia deliver other chemical messages that calm the inflammation, keep the brain healthy and tidy, and the animal’s thinking intact.
But as animals age, recent studies have shown that their microglia can malfunction, causing inflammation, but then failing to calm it down, leading to continuous brain inflammation. This chronic inflammation can kill healthy cells and cause problems with memory and learning, sometimes severe enough to cause a rodent version of Alzheimer’s disease.
Unless the animals play sports. In that case, post-mortem examination of their tissues shows that well into old age the brains of the animals generally teem with healthy, helpful microglia, showing little sign of ongoing encephalitis, while the older rodents themselves retained a youthful ability to learn. and to remember.
We’re not mice, though, and even though we have microglia, scientists hadn’t previously found a way to investigate whether being physically active as we age — or not — would affect the inner workings of microglial cells. So for the new study, published in November in the Journal of Neuroscience, scientists at Rush University Medical Center in Chicago, the University of California, San Francisco and other institutions used data from the ambitious Rush Memory and Aging Projection. For that study, hundreds of Chicago residents, most of them in their early 80s, took extensive annual thinking and memory tests and wore an activity monitor for at least a week. Few exercised formally, the monitors showed, but some moved or walked much more often than others.
Many of the participants died as the study continued, and the researchers examined stored brain tissue from 167 of them, looking for persistent biochemical markers of microglial activity. They basically wanted to see if people’s microglia appeared to be constantly overstimulated during their final years, causing brain inflammation, or being able to reverse their activity when needed, blunting inflammation. The researchers also looked for common biological features of Alzheimer’s disease, such as the telltale plaques and tangles that traverse the brain. They then compared this data with information from people’s activity trackers.