Aspirin Enhances Autophagy to Reduce Amyloid in Mouse Models of Alzheimer's
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.
Link: https://www.rush.edu/news/press-releases/can-aspirin-treat-alzheimers
Good to know. I take 2 low dose aspirin per day along with fish oil and a mens 50+ multi-vitamin. Probable some of these are expensive urine, though.
Article on restoring normal phenotype in progeria through blocking acetyltransferase NAT10, same behavior seen in aged phenotype, could lead to interesting pathway:
http://stke.sciencemag.org/content/11/537/eaar5401
Well it would be pretty easy to do a meta-study and check the statistics of human Alzheimer's patients using aspirin vs the ones who could not. Also what about ibuprofen and paracetamol ? They are considered stronger and better aspirin replacement. I would not be surprised if there are studies doing such correlation
And I wouldn't be surprised if there is no statistically significant effect. Or at least not a large one. After all there is so much aspirin usage that a strong effect in humans would have been noticed by now
Aspirin has been shown to have life extension benefits in a number of studies. Like Robert above, I take the equivalent of 2 small aspirins/day for life extension. You may want to take white willow bark, which does not have the acidic qualities of aspirin if you are at all sensitive to bleeding in the GI tract.
How about boswellia does anyone have any idea about it does it work like aspirin ?
How about aspirin internal bleeding and increased risk of stroke?