Dementia does not arrive all at once.

It begins quietly, often invisibly, as small disruptions in how brain cells communicate with one another. Signals misfire. Messages arrive late or not at all. Over time, those damaged connections lead to structural changes in the brain itself, including shrinkage in regions responsible for memory, reasoning, and behavior. What people experience outwardly—forgetfulness, confusion, personality changes—is the final expression of a process that may have been unfolding for years or even decades.

Because of this slow progression, dementia has long been understood as a condition shaped by many overlapping factors. Genetics play a role, but so do age, cardiovascular health, metabolic conditions, lifestyle choices, sleep, education, and long-term exposure to stress or inflammation. Increasingly, researchers are also examining whether medications taken over long periods might subtly influence cognitive health in ways not fully understood when those drugs were first approved.

One medication now drawing renewed scrutiny is gabapentin.

Gabapentin is an FDA-approved drug originally developed to treat seizures and certain types of nerve pain. Over time, its use expanded far beyond those original indications. Today, gabapentin is commonly prescribed—often off-label—for a wide range of conditions, including fibromyalgia, sciatica, chronic pain syndromes, restless legs, insomnia, anxiety, and even menopausal symptoms.

Part of gabapentin’s appeal lies in its reputation. Compared with opioids, benzodiazepines, and some sleep medications, gabapentin has been viewed as less addictive and relatively safer for long-term use. As concerns about opioid dependence grew, gabapentin increasingly became a go-to alternative for managing chronic discomfort and neurological symptoms.

But “less addictive” does not mean “without consequence.”

Clinicians have long noted that gabapentin can produce side effects such as dizziness, fatigue, slowed thinking, memory lapses, difficulty finding words, and impaired coordination. For many patients, these effects are mild or temporary. For others, especially at higher doses or with prolonged use, cognitive symptoms may persist.

Until recently, the long-term implications of those cognitive effects remained uncertain.

That uncertainty is what prompted a new investigation published in Regional Anesthesia & Pain Medicine, where researchers explored whether gabapentin use might be associated with an increased risk of dementia and mild cognitive impairment (MCI).

The study drew on data from the TriNetX health research network, a large database containing anonymized electronic health records from millions of patients. Researchers identified more than 26,000 adults and divided them into two groups: those who had been prescribed gabapentin and those who had not.

Rather than focusing on short-term exposure, the researchers examined prescription patterns over time. This allowed them to assess whether repeated gabapentin use correlated with later diagnoses of dementia or MCI.

What they found was striking.

Individuals who had received six or more gabapentin prescriptions showed a 29% higher risk of developing dementia compared with non-users. The risk of mild cognitive impairment was even higher—an increase of 85%.

Perhaps most unexpected was where the strongest association appeared.

The most pronounced increase in risk was not among the oldest patients, but among adults aged 35 to 49. In this group, dementia risk doubled, and the risk of MCI tripled compared with peers who had not used gabapentin.

This finding challenged common assumptions about dementia as a disease almost exclusively tied to advanced age. It raised the possibility that certain medications might influence cognitive trajectories much earlier in life, long before symptoms would typically be expected.

However, the study’s authors were careful to emphasize an essential point: association does not equal causation.

Nafis B. Eghrari, the study’s lead author, noted that while the data reveal a statistical link, they do not prove that gabapentin directly causes dementia or cognitive decline. The findings indicate correlation, not mechanism.

Previous research on gabapentin’s effects on cognition has been mixed. Some studies suggest reversible cognitive slowing, particularly at higher doses. Others find minimal long-term impact. Still others hint at subtle neurological changes that may not become clinically apparent until years later.

This inconsistency highlights one of the greatest challenges in studying dementia risk: isolating the influence of a single factor in a condition shaped by so many variables.

Experts reviewing the study have pointed out several important limitations.

First, the analysis did not fully account for underlying health conditions. People prescribed gabapentin often have chronic pain, neurological disorders, or mental health conditions—many of which are themselves associated with higher dementia risk. Without adjusting for these factors, it is difficult to determine whether gabapentin is a contributor or simply a marker of vulnerability.

Second, the study did not include detailed information on dosage or duration. Six prescriptions could represent vastly different levels of exposure depending on dose strength and how long the medication was taken. A person using low-dose gabapentin intermittently is not equivalent to someone taking high doses daily for years.

Third, other medications were not fully accounted for. Polypharmacy—the use of multiple drugs—is common in people managing chronic conditions, and drug interactions may amplify cognitive effects in ways that are difficult to disentangle.

Lifestyle factors also went unmeasured. Physical activity, sleep quality, education, diet, social engagement, and alcohol use all influence dementia risk. Without incorporating these variables, conclusions must remain cautious.

Still, many clinicians agree that the findings should not be dismissed.

Even without proof of causation, the association raises reasonable concern—especially given how widely gabapentin is prescribed and how early in adulthood some individuals begin taking it.

Some specialists argue that gabapentin’s reputation as a “safe alternative” may have encouraged long-term use without sufficient reassessment. Medications initially intended for short-term symptom relief can quietly become permanent fixtures in a patient’s life, renewed automatically year after year.

This study adds weight to the argument that long-term prescriptions should not be treated as static decisions.

Researchers and clinicians alike are now calling for regular cognitive monitoring in patients who take gabapentin over extended periods. Simple screening tools can detect early changes in memory, attention, and executive function—changes that patients themselves may normalize or overlook.

Patients are also encouraged to report subtle cognitive symptoms rather than dismiss them as stress, aging, or fatigue. Difficulty recalling words, trouble concentrating, or feeling mentally “slower” may warrant discussion, especially if symptoms emerge after starting or increasing a medication.

Importantly, experts stress that patients should not stop taking gabapentin abruptly based on this study alone. Sudden discontinuation can cause withdrawal symptoms, increased pain, or seizure risk in vulnerable individuals. Any changes should be made in consultation with a healthcare provider.

Future research aims to answer the questions this study cannot.

Does gabapentin directly contribute to neurodegeneration, or does it unmask vulnerabilities already present? Are certain doses or durations riskier than others? Do age, genetics, or coexisting conditions modify the effect? And most critically, are any cognitive changes reversible if the medication is reduced or discontinued?

Until those answers emerge, the study serves as a reminder of something medicine continually relearns: drugs approved for one purpose can have consequences beyond their original scope, especially when used widely and long-term.

Gabapentin remains an effective and valuable medication for many people. For some, it significantly improves quality of life. But as this research suggests, its benefits—like those of all medications—must be weighed against potential long-term risks.

In the end, the conversation is not about fear, but about awareness.

Dementia develops slowly. So do the decisions that may influence its course. Recognizing possible risks early allows patients and clinicians to make more informed, individualized choices—before subtle changes become permanent ones.