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"The results of our study identify a possible new role for one of the most widely used, common and over-the-counter drugs in the world," said Kalipada Pahan, a professor at Rush University Medical Center in the United States. -United.
Although the exact cause of the progression of Alzheimer's disease is unknown, the impaired clearance of toxic beta-amyloid, particularly the hippocampus, is a major mechanism.
The activation of the cellular machinery responsible for eliminating brain waste has therefore emerged as a promising strategy for slowing down the disease.
Beta-amyloid forms aggregates called amyloid plaques, which damage connections between nerve cells and are one of the major signs of Alzheimer's disease.
Published in The Journal of Neuroscience, the study shows that aspirin decreases the pathology of amyloid plaque in mice by stimulating animal cell component lysosomes that help remove cell debris.
"Understanding how the plaques are eliminated is important for developing effective drugs that stop the progression of Alzheimer's disease," Pahan said.
A protein called TFEB is considered the main regulator of waste disposal.
Researchers gave aspirin orally for one month to genetically modified mice with Alzheimer's disease, then badessed the amount of amyloid plaque in the most affected parts of the brain by Alzheimer's disease.
They discovered that aspirin-based drugs increased TFEB, stimulated lysosomes, and decreased the pathology of amyloid plaque in mice.
"This study adds another potential benefit to the already established uses of aspirin for the relief of pain and for the treatment of cardiovascular disease," Pahan said.
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