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We know that obesity is bad for the brain. Obese people tend to have inflammation in their brains, which can lead to decreased cognitive function and increased risk of developing disorders such as dementia or Alzheimer’s disease. What we don’t yet know is the exact mechanism of how obesity causes these cognitive impairments.
We do know bits and pieces, like that obesity causes the loss of synapses, which are the connections between brain cells. Synapse loss is a normal developmental process and when a synapse is no longer needed it is destroyed up by microglia, the immune cells of the brain. Obesity is also known to increase the activity of microglia. This leads to the question, which way does this relationship go? Does obesity increase the rate of synapse loss, causing microglia to increase their activity to keep up, or does obesity put microglia into overdrive and cause them to destroy needed synapses?
To answer this question, researchers from Princeton University compared the mental functioning of obese and lean mice. As expected based on the previous research I outlined above, obese mice had impaired learning and memory compared to lean mice, as well as fewer synapses and more microglia. When the researchers then reduced the number or activity of microglia, they prevented both the learning deficits and the synapse loss in obese mice. Reducing the activity of microglia caused no changes in the lean mice (probably because their microglia weren’t very active to begin with). These results suggest that overactive microglia destroying needed synapses was the cause of the obesity-related learning impairments.
This study provides the first experimental evidence that microglia are not just bystanders, but play an active role in obesity-related cognitive impairment. This suggests that someday, we could use drugs that target microglia in order to treat cognitive impairment in obese human patients.