Taking a low-dose aspirin once a day does not reduce the risk of developing MCI – dementia – Alzheimer’s disease


Taking a low-dose aspirin once a day does not reduce the risk of thinking and memory problems caused by mild cognitive impairment or probable Alzheimer’s disease, nor does it slow the rate of cognitive decline, according to a large study published in the March 25, 2020, online issue of Neurology.

Aspirin has anti-inflammatory properties and also thins the blood. For years, doctors have been prescribing low-dose aspirin for some people to reduce their risk of heart disease and stroke.

However, there are also possible risks to taking aspirin, including bleeding in the brain, so guidance from a doctor is important.

Because aspirin can be beneficial to the heart, researchers have hypothesized, and smaller previous studies have suggested, that it may also be beneficial to the brain, possibly reducing the risk of dementia by reducing inflammation, minimizing small clots or by preventing the narrowing of blood vessels within the brain.

“Worldwide, an estimated 50 million people have some form of dementia, a number that is expected to grow as the population increases, so the scientific community is eager to find a low-cost treatment that may reduce a person’s risk,” said study author Joanne Ryan, PhD, of Monash University’s School of Public Health in Melbourne, Australia.

“Unfortunately, our large study found that a daily low-dose aspirin provided no benefit to study participants at either preventing dementia or slowing cognitive decline.”

The study involved 19,114 people who did not have dementia or heart disease. A majority of participants were age 70 or older.

They took thinking and memory tests at the start of the study as well as during follow-up visits.

Half of the people were given daily 100 milligram low-dose aspirin while the other half were given a daily placebo. They were followed for an average of 4.7 years, with annual in-person examinations.

Over the course of the study, 575 people developed dementia.

Researchers found no difference between those who took aspirin and those who took placebo in the risk of developing mild cognitive impairment, dementia, or probable Alzheimer’s disease. There was also no difference in the rate of cognitive change over time.

Half of the people were given daily 100 milligram low-dose aspirin while the other half were given a daily placebo. They were followed for an average of 4.7 years, with annual in-person examinations.

“While these results are disappointing, it is possible that the length of just under five years for our study was not long enough to show possible benefits from aspirin, so we will continue to examine its potential longer-term effects by following up with study participants in the coming years,” said Ryan.

A limitation of the study was that only relatively healthy people were enrolled, and such a population may benefit less from aspirin than the general population.

Funding: The study was supported by the National Institute on Aging, the National Cancer Institute and the National Institutes of Health in the United States, the Australian National Health and Medical Research Council, Monash University and the Victorian Cancer Agency. Bayer, the maker of the drug, provided the trial drug and placebo but had no other role in this trial.

Alzheimer’s disease (AD) is the most common cause of dementing illnesses in elderly patients [1]. It is a degenerative brain disease, presenting with the characteristic features of cognitive difficulties, memory problems; challenges with learning and problem solving; and ultimately difficulty in speaking, swallowing, and walking [2].

A central role for inflammation has been implicated in the pathogenesis of AD [3]. This idea is evidenced by the increased activity of microglial cells, correlative with the severity of symptoms; as well as role of various inflammatory mediators in neurodegeneration, dysfunction of glial supportive cells and amyloidosis [4].

Adaptive immunity, as well as communication between central and peripheral immune systems, have also been implicated in the neuroinflammation associated with AD [5].

There is evidence to suggest that inflammation occurs before the clinical onset of AD, and several AD candidate genes for inflammation have been identified as well, further supporting this premise [6].

No treatment options are currently available to reduce or offset the risk posed by neuronal destruction in the progression of AD.

The six drugs currently approved by the Food and Drug Administration (FDA), including Rivastigmine, Galantamine, Donepezil, Memantine, Memantine combined with Donepezil, and Tacrine, only offer symptomatic relief [1].

Keeping in view this central role of inflammation, various anti-inflammatory treatments in AD have shown efficacy with varying results after the conduction of many clinical trials. Non-steroidal anti-inflammatory drugs (NSAIDs) form the cornerstone of these treatments, which work mainly by inhibiting cyclo-oxygenase (COX) enzyme activity, which is responsible for the neuroinflammatory response prevalent in AD [3].

NSAIDs also maintain mitochondrial Ca2+ homeostasis and target Rho-GTPases (guanosine triphosphate) and peroxisome proliferator-activated receptors (PPARs); the latter pathways are associated with axon growth, tau protein phosphorylation, and astrocyte motility, all of which play a role in the pathogenesis of AD [7].

Furthermore, certain NSAIDs, including Sulindac, Ketorolac, Ibuprofen, and Naproxen among others, act as inhibitors of amyloid-β ( A-β) aggregation, a contributing event in the development of AD, by working as A-β fibril inhibitors in terms of predicted binding affinity [8].

While epidemiologic studies have shown a reduced incidence of AD with NSAIDs use, randomized clinical trials (RCTs) have failed to show promising results with NSAIDs in AD patients [3,9].

This, in part, has been attributed to the low number of RCTs conducted, the lack of a long-term, large-scale RCT using cognitive measures [3], and limitations in the studies held so far regarding duration and dose of NSAIDs used.

Therefore, NSAIDs are currently not recommended for either prevention or treatment of AD [9].

This literature review aims to point out the discrepancies that exist between observational studies and RCTs regarding the role of NSAIDs in limiting the progression of AD.

It also seeks to provide recommendations for the use of NSAIDs as well as novel anti-inflammatory drugs in AD patients. 



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