Long-term gabapentin use is associated with an increased risk of dementia, though researchers haven’t proven it directly causes the condition. The largest study to date, covering more than 200,000 patients in Taiwan, found that people who used gabapentin or its close relative pregabalin were 45% more likely to develop dementia than matched non-users. A separate study focused on chronic low back pain patients found a similar pattern: those with six or more gabapentin prescriptions had a 29% higher incidence of dementia. The risk appears to climb with higher doses and longer use.
What the Population Studies Show
Two major observational studies have examined this question, and both point in the same direction. In the Taiwanese study, which followed 34,467 gabapentin or pregabalin users and 172,335 non-users over an average of nearly five years, the dementia incidence rate was 981 per 100,000 person-years in the exposed group compared to 605 per 100,000 in the unexposed group. That translated to a 45% higher risk after adjusting for other health conditions.
A more recent study of 26,416 adults with chronic low back pain found that patients prescribed gabapentin six or more times had a 29% higher risk of dementia and an 85% higher risk of mild cognitive impairment compared to those not prescribed the drug. Patients who received 12 or more prescriptions faced even steeper odds: a 40% increase in dementia risk and a 65% increase in mild cognitive impairment.
These are observational studies, which means they can identify a statistical link but can’t definitively prove gabapentin caused the dementia. People who take gabapentin often have chronic pain, epilepsy, or other conditions that may independently affect brain health. Still, both studies controlled for common confounding factors like age, diabetes, and cardiovascular disease, and the association held.
Higher Doses Carry Greater Risk
One of the most striking findings is a clear dose-response pattern. The Taiwanese study divided patients into groups based on their cumulative drug exposure over the follow-up period. Compared to those with the lightest use, people in the second-lowest tier had a 24% higher dementia risk. Those in the next tier had a 69% higher risk. And people with the highest cumulative exposure had a 144% higher risk of developing dementia. This kind of staircase pattern, where more drug use correlates with more risk in a consistent way, strengthens the case that the association isn’t simply a statistical coincidence.
Younger Adults May Be More Vulnerable
Counterintuitively, the relative risk increase appears larger in younger people. In the Taiwanese data, gabapentin or pregabalin users under age 50 had more than three times the dementia risk of non-users in the same age group. For users aged 50 to 59, the risk was about 58% higher. For those 60 to 69, it was 54% higher, and for those 70 and older, 30% higher.
The chronic low back pain study echoed this pattern. Non-elderly adults (ages 18 to 64) prescribed gabapentin had more than twice the risk of dementia and two and a half times the risk of mild cognitive impairment compared to those not prescribed the drug. Because dementia is rare in younger adults, even a small absolute increase can look dramatic in relative terms. But the consistency of this finding across two independent studies is notable, and researchers have flagged it as a particular concern.
How Gabapentin Might Affect the Brain
Gabapentin works by binding to a specific protein on nerve cells that plays a role in how new connections between brain cells are formed. Research published in Cell found that gabapentin powerfully blocks the formation of excitatory synapses, the connections that allow brain cells to communicate and that are essential for learning and memory. It does this by interfering with a signaling process that a protein called thrombospondin uses to trigger new synapse growth.
This mechanism is actually part of how gabapentin treats pain and seizures: it prevents the brain from forming excess connections that contribute to those conditions. But over months or years, chronically suppressing the brain’s ability to build new synapses could plausibly impair the neural plasticity needed to maintain healthy cognition. This is a theoretical concern supported by laboratory and animal data, not yet confirmed in human brain studies, but it offers a biologically plausible explanation for the population-level findings.
Short-Term Cognitive Side Effects
Even in the short term, gabapentin affects thinking. In FDA clinical trials for epilepsy, 2% of patients taking gabapentin reported memory problems (amnesia) compared to 0% on placebo. Common side effects like drowsiness and dizziness, which are well-documented, can also cloud thinking.
A small study of patients with spinal cord injuries found measurable cognitive declines within the first week of starting gabapentin. By four weeks, scores on five of nine cognitive tests had improved compared to the one-week mark, suggesting the brain partially adapts to the drug over time. This adaptation is encouraging for short-term users, but it doesn’t address whether years of use carry a cumulative toll on brain function that goes beyond these initial side effects.
Older Adults Face Compounding Risks
Gabapentin is cleared from the body through the kidneys, and kidney function naturally declines with age. This means older adults tend to have higher drug levels in their blood at the same dose, intensifying both therapeutic and side effects. On top of that, older adults are more likely to take multiple medications. The American Geriatrics Society’s Beers Criteria, a widely used list of drugs that warrant caution in older adults, flags gabapentin specifically when used alongside opioids due to risks of excessive sedation and respiratory depression. The FDA has issued similar warnings about combining gabapentin with antidepressants, particularly in older patients.
These drug interactions matter for cognitive health because sedation, reduced oxygen levels from respiratory depression, and the cumulative burden of multiple brain-active medications can all contribute to confusion and cognitive decline, potentially compounding whatever independent risk gabapentin itself carries.
What This Means If You Take Gabapentin
The evidence so far is concerning but not conclusive. No randomized controlled trial has tested whether gabapentin directly causes dementia, and such a trial would be difficult to conduct ethically. What exists are two well-designed population studies showing a consistent, dose-dependent association, and a plausible biological mechanism that could explain it.
If you’ve been taking gabapentin for years and notice memory problems, fogginess, or difficulty concentrating, those symptoms are worth bringing up with your prescriber. The short-term cognitive effects of the drug appear to be at least partially reversible, based on the limited data available, but no study has tracked whether cognitive function fully recovers after stopping long-term use.
The dose-response relationship is particularly relevant for anyone weighing their options. The data suggest that lower cumulative exposure is associated with less risk. For some people, gabapentin remains the best available treatment for their condition. For others, especially those on high doses for extended periods, the emerging evidence may tip the balance toward exploring alternatives.