Study shows that inflammation in the brain may be key to Alzheimer’s

According to the professor, this evidence had already been found in animals and in post-mortem brains, but scientists had never seen this communication between cells in living patients. This finding was possible due to the use of markers such as state-of-the-art imaging tests and ultrasensitive biomarkers.

“We already knew that the beta-amyloid plaque (the stones that cause inflammation) made the astrocyte reactive. What we didn’t know is that for the disease to be established, the microglia also had to be reactive. So, with these two active cells, the astrocyte associates with the beta-amyloid plaque. If the astrocyte is reactive and the microglia is not, nothing happens. In this context of the two active cells, we were able to explain the entire progression of the disease with the other markers, of amyloid and tau up to 76% of the variance in cognition,” he said.

Zimmer highlighted that it is not yet known exactly what causes the appearance of beta-amyloid plaque, however it is known that there are several risk factors and that the combination of genetics and exposure throughout life (exposome) influence it. The more good exposures, the lower the chances of developing Alzheimer’s in the future.

Among the risk factors for Alzheimer’s are smoking, alcoholism, a sedentary lifestyle, obesity, among others. On the contrary, they contribute to avoiding physical activities, good nutrition, quality of sleep, and intellectual stimulation.

The discovery contributes to a new vision of treatment for the disease, as in recent years the idea was to develop drugs that act on beta-amyloid plaques. The new perspective suggests that it may be necessary to develop drugs that can interrupt communication between astrocytes and microglia.

“So the idea is that, in addition to removing the ‘pebbles’, we will need to calm this information in the brain, calm this dialogue between the two cells”, he explained.