Rheumatoid Arthritis Patients Have a Higher Risk of Dementia, But Biologics Could Help Lower It

In recent years a number of studies have identified a connection between inflammation and various types of dementia, including Alzheimer’s disease. Meanwhile, people with rheumatoid arthritis (RA) — an inflammatory autoimmune condition — are more apt than others to develop dementia as they get older. So, can treating RA with biologic drugs that block inflammatory proteins mitigate this risk?

Research presented at ACR Convergence 2020, the American College of Rheumatology’s annual (virtual) meeting, suggests that it may be possible.

Although this study does not directly prove that biologic drugs prevent dementia, the researchers found compelling evidence that biologic drugs might reduce an RA patient’s risk of age-related memory issues.

The study, which was led by Sebastian Sattui, MD, a rheumatologist at Hospital for Special Surgery in New York City, relied on Medicare claims data that was submitted between 2006-2017. The researchers identified more than 140,000 RA patients who were enrolled in Medicare for at least one year and had no history of dementia when the study began.

During the study period, nearly 3,800 of these RA patients developed dementia. The researchers determined that the incidence of dementia was significantly higher among RA patients who were being treated with a conventional DMARD (disease modifying anti-rheumatic drug), such as methotrexate, than it was among those who were on a biologic drug like infliximab (Remicade) or etanercept (Enbrel).

Patients on any biologic drug were 17 percent less likely than those using only a traditional DMARD to have developed dementia.

There are many different classes of biologics that are approved to treat RA, including TNF inhibitors, IL-1 blockers, IL-6 blockers, IL-17 blockers, B-cell inhibitors, and T-cell inhibitors. There are also other kinds of targeted therapies called JAK inhibitors. All of these medications work differently from each other, but they act on specific immune system pathways to reduce inflammation.

Because patients in this study fared equally well regardless of which class of biologic drug they were taking, the authors suggested that a specific mechanism of action (such as targeting TNF or IL-6) is unlikely to be responsible for reducing dementia risk.

Instead, they theorized that people taking biologics — despite generally have more severe disease than those who only use conventional DMARDs — were probably benefitting from the “overall decrease in inflammation” that biologics provide.

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