They infused the brain of dementia-bred animals with a concentrated dose of irisin. These mice soon showed better results in memory tests and showed signs of improved synaptic health.
At the same time, they soaked the brains of healthy animals with a substance that inhibits the production of irisin, and then pumped them in the form of beta amyloid, a protein that accumulates to form plaques in the brains of people with Alzheimer's disease. In fact, they gave the mice dementia. And without iris in the brain, the once-healthy mice soon showed signs of memory deterioration and malfunction in the synapses between the neurons in their hippocampus.
Finally and perhaps most importantly, the scientists trained healthy mice that swam for nearly one hour for five weeks for five weeks. Previously, some animals were also treated with the substance that blocks the production of irisin. In the untreated animals, irisin levels in the brain flourished during training and later, after the animals' brains were exposed to beta-amyloid, these seemed to ward off its effects and perform significantly better in memory tests than sitting control mice, as well had been exposed.
But the animals that could not make irises did not benefit much from exercise. After beta-amyloid exposure, they were about as bad at memory tests as sedentary animals with beta-amyloid in the brain. Overall, these experiments suggest that movement may protect against dementia by causing some of the increase in the amount of irisin in the brain, says Ottavio Arancio, a professor of pathology and cell biology at Columbia University, who co-researched with two Dozens of colleagues from the Brazilian Federal University of Rio de Janeiro, who has conducted Queen's University in Canada and other institutions. 19659008]