Scientists have found that aspirin cooperates with some subcellular mechanisms in the brain to prevent the formation of amyloid plaques, which are sticky protein blocks around brain cells and are considered as the main cause of Alzheimer's disease. According to this new study on mice,
In this study, mouse experiments show that aspirin enhances the ability of lysosomes to remove amyloid plaques or prevent them from forming. Lysosomes are a bit like waste disposers and recyclers for cells. The researchers published their findings in the Journal of Neuroscience today (June 2), saying that aspirin should have the same effect on human Alzheimer's disease.
According to the data of the Centers for Disease Control and Prevention, Alzheimer's disease is the most common dementia and a progressive brain disease, which affects nearly 6 million Americans and is the sixth leading cause of death for all adults in the United States. At present, there is no cure, and the success of drug therapy in slowing down the progress of the disease is very limited. [9 surprising risk factors for dementia]
Aspirin, also known as acetylsalicylic acid, is a cheap drug with a century-long history of low-dose safety, except for possible gastric bleeding and small risk of internal bleeding. Many adults take small doses of aspirin as a mild blood thinner every day to help prevent heart attacks.
In fact, several national studies on aspirin and heart health have found that aspirin can also reduce the risk of Alzheimer's disease, albeit to a limited extent. A meta-analysis published by China researchers in Frontiers of Geriatric Neuroscience from March 2065438 to March 2008 reviewed 18 whole population studies and found that frequent use of non-steroidal anti-inflammatory drugs (NSAIDs) including aspirin can reduce the average risk by 20%.
Aspirin and Alzheimer's Harmo's disease are based on the possible link between aspirin and prevention of Alzheimer's disease. It was first observed more than ten years ago that researchers at Rush University Medical Center in Chicago carefully designed an experiment to give aspirin to mice with Alzheimer's disease, and directly applied aspirin to mouse brain cells cultured in the laboratory.
The first author, Kalipada Pahan, a professor of neuroscience at a university, said that both in vivo and in vitro methods seemed to prevent or reverse Alzheimer's disease. Pahan explained that "KDSP" and "KDSP" aspirin activate a cell receptor called PPARα, which in turn regulates a protein called TFEB, which is the main regulator of lysosomal activity. In short, aspirin helps cells remove cellular debris, including protein, which forms amyloid plaques. [5 interesting facts about aspirin]
"We hope to see similar results in human brain cells," Pachan told Life Science.
Pachan said that in fact, other drugs, such as the triglyceride lowering drug Gefilozzi (sold as Lopid), are also targeted at TFEB, but aspirin is safe and can be purchased without prescription, with fewer side effects.
Rajini Rao, a professor of physiology at Johns Hopkins University School of Medicine in Baltimore, who was not involved in the study, said that the new study "provides an elegant mechanical explanation for the protective effect of aspirin on cells and animal models."
However, she pointed out that Rao told Life Science that it is not clear whether the improvement of amyloid clearance will translate into better brain function.
"The epidemiological findings of taking aspirin and dementia are mixed." At the same time, there are some signs that it has a protective effect, which other studies have failed to replicate. Unfortunately, in fact, every drug used in the trial of Alzheimer's disease is like this-more than 99% of drugs have failed in clinic-which is why the study of Alzheimer's disease is particularly challenging. Using it every day does bring some risks and should not be used as an unproven method to treat or prevent Alzheimer's disease. He added that for the lysosomal activity of aspirin, the cell receptor PPARα needs to exist, so anyone who lacks enough PPARα receptors for Alzheimer's disease will not benefit from aspirin. Pachan said:
Follow Christopher Wanjek@Wanjek and get daily tweets about health and science, which may explain the mixed results of the whole population study. "。 Jack Wan is the author of Food at Work and Bad Medicine. His column "Bad Medicine" appears regularly in Life Science.