A new study has found that aspirin may reduce the accumulation of amyloid plaques in the brain. The research, at this stage only demonstrated in mouse models, is suggesting that it may lead to the common, over-the-counter drug being utilized therapeutically for treatment of Alzheimer's disease, but some scientists are dubious as to the merits of any broader human applications from this study.
Previous studies have noted a potential connection between aspirin consumption and a lower risk of Alzheimer's disease. The new research, from a team at Rush University Medical Center, set out to better understand what mechanism, if any, might underlie this observation. The study administered a low oral dose of aspirin for one month to mice that had been engineered to have similar pathology to Alzheimer's disease.
The results uncovered a novel mechanism by which aspirin works on the brain to help decrease the volume of accumulated amyloid plaques. By upregulating a protein called TFEB and stimulating lysosomes, the aspirin seemed to effectively help activate the inbuilt cellular processes that work to remove waste from the brain.
"This research study adds another potential benefit to aspirin's already established uses for pain relief and for the treatment of cardiovascular diseases," says Kalipada Pahan, senior author on the study. "More research needs to be completed, but the findings of our study have major potential implications for the therapeutic use of aspirin in AD and other dementia-related illnesses."
While the research in itself is strong, the conclusions about any potential applications are certainly up for debate. Several major recent human trials into drugs that reduce amyloid plaques have notably failed and some researchers are starting to raise doubts over the veracity of the amyloid hypothesis, the primary idea that drives much Alzheimer's research.
As well as this new study only displaying amyloid reducing results in a very small sample size of mice, it did not establish any symptomatic connection to an improvement in dementia-like effects whatsoever. On top of that, there are serious concerns that these kind of results do not translate well from mice to humans.
"A number of compounds have achieved this level of amyloid reduction in mice, yet have subsequently failed in clinical trials in humans," explains Clive Ballard, from the University of Exeter. "The failures may be as a result of the differences between Alzheimer mice and human pathology, and the poor translation of benefits into humans."
Perhaps even more significant is the fact that human clinical trials examining the effect of aspirin in patients with Alzheimer's have already been conducted. As Rob Howard, from University College London explains, "The drug had no beneficial effects on outcome measures and was associated with an increased risk of gastrointestinal haemorrhage."
Ultimately, despite the decent science involved in this new study, this is not in any way a convincing case for aspirin being used to beneficial effect in human Alzheimer's patients. In fact, one study found that Alzheimer's patients using aspirin may be at higher risk for intracerebral hemorrhage. So while headlines may be currently circulating asking rhetorically whether aspirin can treat Alzheimer's, the answer at this stage is most surely … no.
The new study was published in the journal JNeurosci.
Source: Rush University Medical Center
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