A number of groups advocate the use of NSAIDs such as aspirin as a means to reduce risk and postpone the development of Alzheimer's disease, based on the evidence accumulated in the past few decades. Aspirin is considered by some to be a calorie restriction mimetic that enhances autophagy, the cellular housekeeping mechanism that is required for calorie restriction to extend life in laboratory species. That said, I normally mention aspirin as a way to dampen excess enthusiasm for any new calorie restriction mimetic, autophagy-stimulating compound demonstrated to slow aging in the laboratory. After all, aspirin slows aging too, and to a similar degree, when tested in short-lived species. We shouldn't expect any of the current crop of allegedly age-slowing compounds that influence these mechanisms to do much more for human health than aspirin has achieved. All sorts of beneficial effects will be observed, such as the one noted here, but at the end of the day the size of the effect matters greatly.
A regimen of low-dose aspirin potentially may reduce plaques in the brain, which will reduce Alzheimer's disease pathology and protect memory. Alzheimer's disease is a fatal form of dementia that affects up to one 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. Poor disposal of the toxic protein amyloid beta in the brain is a leading mechanism in dementia and memory loss. Activating the cellular machinery responsible for removing waste from the brain has emerged as a promising strategy for slowing Alzheimer's disease.
Amyloid beta forms clumps called amyloid plaques, which harm connections between nerve cells and are one of the major signs of Alzheimer's disease. Building on previous studies demonstrating a link between aspirin and reduced risk and prevalence of Alzheimer's disease, researchers were 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.