In a recent study, researchers from Rush University found that low-dose aspirin may help reduce plaques in the brain, which will reduce Alzheimer’s disease and protect memory.
Alzheimer’s disease is a fatal form of dementia that affects up to 1 in 10 Americans age 65 or older.
To date, the FDA has approved very few drugs for the treatment of Alzheimer’s disease-related dementia and the medications that exist can only provide limited symptomatic relief.
The exact cause of Alzheimer’s disease progression is unknown. However, poor disposal of the toxic protein amyloid beta in the brain is a leading mechanism in dementia and memory loss.
A promising strategy for slowing Alzheimer’s disease is activating the cellular machinery responsible for removing waste from the brain.
Amyloid beta forms clumps called amyloid plaques, which harm connections between nerve cells and are one of the major signs of Alzheimer’s disease.
This study tested if there is a link between aspirin and reduced risk and prevalence of Alzheimer’s disease,
The team was able to show that aspirin decreases amyloid plaque pathology in mice by stimulating lysosomes—the component of animal cells that help clear cellular debris.
A protein called TFEB is considered the master regulator of waste removal.
The researchers gave aspirin orally for a month to genetically modified mice with Alzheimer’s pathology, then evaluated the amount of amyloid plaque in the parts of the brain affected most by Alzheimer’s disease.
They found that the aspirin medications augmented TFEB, stimulated lysosomes and decreased amyloid plaque pathology in the mice.
The researchers said the results of the study identifies a possible new role for one of the most widely used, common, over-the-counter medications in the world.
Understanding how plaques are cleared is important to developing effective drugs that stop the progression of Alzheimer’s disease.
This research study adds another potential benefit to aspirin’s already established uses for pain relief and for the treatment of cardiovascular diseases.
More research needs to be completed, but the finding has major potential implications for the therapeutic use of aspirin in AD and other dementia-related illnesses.
The finding is published in The Journal of Neuroscience.
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