Anticoagulants, normally taken to prevent stroke in patients with atrial fibrillation, may also help to stave off dementia.
The new study was carried out by Leif Friberg and Mårten Rosenqvist, from the Karolinska Institute in Stockholm, Sweden. They started out from the already established link between atrial fibrillation (A-fib) and dementia.
A-fib is a common form of irregular heartbeat, or arrhythmia, and studies have shown that patients living with it have a considerably higher risk of developing dementia, including Alzheimer's disease.
Other studies have added that this association has nothing to do with the blood-thinning treatment that most A-fib patients are on.
But the precise role of anticoagulant, or blood-thinning, drugs on dementia risk is not yet known and has not been sufficiently investigated, explain the authors.
One theory suggests that, since anticoagulants prevent stroke by protecting against large blood clots, they should also prevent dementia by protecting against the small blood clots and microinfarctions that characterize it.
To explore this hypothesis, Friberg and Rosenqvist examined the incidence of dementia among patients with A-fib, comparing patients who took anticoagulants with those who did not.
The researchers also wanted to see whether or not the type of anticoagulant made any difference — such as whether newer blood thinners had a different effect on dementia risk when compared with old ones.
Dementia risk cut by nearly half
To this end, Friberg and Rosenqvist reviewed the history of 444,106 Swedish patients with A-fib between 2006 and 2014. At the beginning of the study, 54 percent of these patients were not taking oral blood thinners. During the study period, 26,210 of all patients developed dementia.
A-fib patients who were on a blood-thinning treatment at the beginning of the study were 29 percent less likely to develop dementia than those who were not.
Also, an "on-treatment analysis" revealed that patients who continued to take the anticoagulants had a 48 percent lower risk of dementia.
Parkinson's disease, alcohol abuse, and the absence of a blood-thinning treatment seemed to be the "strongest predictors for dementia."
The findings provide strong evidence that oral blood thinners may prevent dementia in patients with A-fib. "In order to prove this assumption," they explain, "randomized placebo controlled trials would be needed, but [...] such studies cannot be done because of ethical reasons."
"It is not possible to give placebo to [A-fib] patients and then wait for dementia or stroke to occur," write Friberg and Rosenqvist.
Finally, the study found no difference between warfarin — which represents an older generation of anticoagulants — and newer ones.
'Use anticoagulants if diagnosed with A-fib'
Friberg comments on some of the clinical implications of the findings, saying, "Patients start on oral anticoagulation for stroke prevention, but they stop after a few years at an alarmingly high rate. In the first year, approximately 15 percent stop taking the drugs, then approximately 10 percent each year."
"Doctors should not tell their patients to stop using oral anticoagulants without a really good reason," he cautions.
"Explain to your patients how these drugs work and why they should use them," Friberg advises. "An informed patient who understands this is much more likely to comply and will be able to use the drugs safely and get better benefits."
"To patients," he continues, "I would say 'don't stop unless your doctor says so. Have your doctor explain why you should take the drug so that you feel you understand and agree.'"
"If you know that [A-fib] eats away your brain at a slow but steady pace and that you can prevent it by staying on treatment, I think most [A-fib] patients would find this a very strong argument for continuing treatment."
"No brain can withstand a constant bombardment of microscopic clots in the long run. [...] [To] preserve what you've got, you should take care to use anticoagulants if you are diagnosed with [A-fib], as they have been prove[n] to protect against stroke and, which this study indicates, also appear to protect against dementia."
The authors also note some of the limitations of their research. Firstly, given that the study only describes an association, it cannot explain causality.
A further limitation was the incomplete medical histories of the patients, which means that the researchers did not have access to information about other potential diseases.
Additionally, the authors note, dementia is a slow-progressing disease that goes undetected for years, which means that its prevalence may have been higher than what the patients reported.