Melatonin is one of the most commonly used sleep aids, which is why many people wonder if it might also be harmful. Questions like "Does melatonin cause dementia?" often arise when people see conflicting headlines and social media posts. Some sources raise concerns about dementia risk, while others highlight research suggesting that melatonin may be linked with changes in sleep disturbances or cognitive health in certain groups.

These concerns are understandable because sleep problems, aging, and cognitive decline often co-occur. Poor sleep can affect memory, disrupt circadian rhythms, and be associated with changes in cognitive function. At the same time, many studies continue to explore how melatonin production and melatonin supplementation show up in people with neurodegenerative diseases such as Alzheimer’s disease.

Examining the actual findings of clinical trials, observational studies, and review and meta-analysis papers can provide a clearer picture. The sections below describe how melatonin works, summarize the current research on melatonin and dementia risk, and outline cautious approaches to discussing melatonin as part of a comprehensive sleep plan.

Melatonin is a hormone produced by the pineal gland that helps signal the body when it is time to prepare for sleep. Its levels typically rise in the evening and fall toward morning, which helps regulate sleep–wake cycles, sleep timing, and overall sleep quality.

Melatonin production depends strongly on light exposure. As daylight fades, melatonin synthesis usually increases, providing one of several cues that support non-rapid eye movement (NREM) sleep, rapid eye movement (REM) sleep, and circadian processes involved in cognitive function and daytime alertness. These rhythms are often examined in research on sleep disorders.

Melatonin levels tend to decline with age, and studies show this decrease can be more pronounced in older adults and in people with Alzheimer’s disease. In fact, lower melatonin levels and melatonin deficiency have been observed alongside higher rates of sleep disturbances in individuals with dementia and mild cognitive impairment, which is one reason researchers have studied melatonin as a potential tool for addressing sleep-related symptoms in these groups. However, these associations do not show that one directly causes the other.

Due to these findings, melatonin supplementation has been investigated in certain sleep medicine and research settings to assess its impact on sleep disturbances in individuals with cognitive impairment.

Concerns that melatonin might increase dementia risk often stem from confusion about different types of sleep aids. Melatonin is sometimes discussed in the same breath as prescription sleep medications, even though their mechanisms and risk profiles differ.

Online discussions about melatonin treatment often mix it together with other sleep aids used in sleep medicine. Some prescription medications, such as certain benzodiazepines, have been associated in observational research with increased risk of dementia in older adults. Melatonin, however, is a dietary supplement with a different action in the central nervous system, and current data do not show the same pattern of risk factors. When these products are grouped together, it can create worry that does not reflect the specific evidence for melatonin.

A Cochrane systematic review of melatonin treatment in dementia patients examined five randomized controlled trials and found that these studies primarily assessed cognition, mood, behavior, and daily function, rather than new cases of dementia or long-term dementia risk. In three of the clinical trials, the pooled Mini-Mental State Examination (MMSE) and ADAS-cognitive scores showed no significant cognitive benefit from melatonin treatment at the administered melatonin dosage.

Two of the trials, using 2.5 mg of melatonin for seven weeks and 3 mg for four weeks, reported statistically significant improvements on certain psychopathological behavior and mood scales, such as measures of agitation, depressive symptoms, anxiety, hallucinations, irritability, and appetite disturbances in dementia patients. In contrast, one study that followed participants for one year found a significant worsening in positive affect on one mood scale, while most other outcomes for mood, behavior, and activities of daily living were non-significant. Across the dementia sleep and behavior trials included in the review, no melatonin-related adverse events were reported. 

Still, the authors concluded that evidence did not support melatonin as an effective treatment for cognitive impairment in people with dementia and that effects on psychopathological behaviors were limited to specific short-term studies, with no data on long-term dementia risk for the general public.

Prescription sleep medications can slow brain activity in a way that may be associated with confusion or falls in older adults. In contrast, melatonin supplements are usually studied for their relationship to circadian rhythms and sleep-wake patterns, not as strong sedatives. Research suggests that concerns about increased risk of dementia largely come from data on certain sleep medications rather than from randomized controlled trials of melatonin therapy itself. Still, experts recommend individual assessment before taking melatonin, especially in older adults with sleep issues or cognitive impairment.

Available research does not show that melatonin causes dementia, although it also has not proven that melatonin prevents dementia. Most human studies focus on sleep quality, oxidative stress markers, circadian rhythms, and short- to medium-term changes in cognitive performance.

Clinical trials and randomized controlled trials involving melatonin supplementation report mixed results. Some studies in adults with mild cognitive impairment or those with dementia describe modest changes in cognitive performance scores or improvements in certain dementia-related sleep measures, such as sleep efficiency or time spent asleep. Other trials have found little or no difference compared with placebo. These results are specific to the participants and dosing used in each trial and do not guarantee outcomes for healthy adults or the broader population.

Experimental work in cells and animals suggests that melatonin has antioxidant properties and may play a role in cell protection and neuroprotection within the central nervous system. In these controlled models, melatonin is described as helping to counter processes linked to oxidative damage and inflammation, often discussed in relation to reactive oxygen species and early steps in neurodegeneration.

Researchers have also reported that melatonin can be synthesized in the mitochondrial matrix of mouse brain cells, where it activates signaling pathways that limit stress-related cytochrome c release and caspase activation, both of which are involved in cell death.

These findings suggest possible mechanisms by which melatonin could be relevant to neurodegenerative diseases, but they come from specific experimental conditions and do not show that melatonin supplementation in the general public will prevent Alzheimer’s disease or other neurological disorders, so further research is still needed.

Good sleep is closely linked to healthier brain function as people age. Research in older adults has shown that disrupted sleep-wake cycles, reduced non-REM sleep, and sleep fragmentation can interfere with waste clearance in the brain, including the removal of molecules such as amyloid. Amyloid is a protein fragment that can accumulate and form sticky deposits in the brain; these deposits are considered one of the hallmark features studied in Alzheimer’s disease and other neurodegenerative disorders.

The review notes that sleep disturbance can raise cerebrospinal fluid amyloid-beta levels and that poor sleep is associated with processes related to neurodegeneration. Because melatonin helps coordinate circadian rhythms and supports sleep timing, melatonin therapy has been studied as a way to improve sleep quality in older adults and in people with mild cognitive impairment or dementia who have disrupted sleep.

These studies suggest that improving sleep and stabilizing circadian rhythms may support cognitive health indirectly, but they do not show that melatonin prevents dementia. Instead, the evidence indicates that melatonin can improve sleep efficiency, reduce sleep variability, and help regulate the sleep-wake cycle, all of which may play a role in maintaining healthier brain function as people age.

There is limited long-term research on melatonin dosage, melatonin levels over time, supplement quality, and outcomes beyond one to two years. Over-the-counter products can vary in melatonin dosage and purity, which may influence both benefits and adverse effects. Because of this, more research is needed before making broad claims about long-term safety, dementia risk, or melatonin’s benefits in large populations.

Studies suggest that poor sleep may increase dementia risk, although the relationship is complex. The brain relies on consistent sleep to process information and clear waste products, and disruptions in sleep length or sleep quality can be linked with changes in cognitive function.

A study on sleep deprivation by Khan and Al-Jahdali (2023) found that both partial sleep loss and total sleep loss are linked to reduced attention, weaker memory, and slower decision-making. Their work shows that missing key sleep stages interferes with normal brain signaling, making it harder for the brain to stay alert and process information efficiently.

The study also notes that repeated sleep restriction over time leads to greater cognitive impairment than a single night without sleep. Chronic sleep loss disrupts the circadian and homeostatic systems that regulate the sleep–wake cycle, which can further weaken concentration and thinking skills. While these findings show clear associations, they do not establish long-term disease outcomes.

Deep non-REM sleep, often called deep sleep, is when the brain’s waste-clearing system works at its highest level. A mouse study using two-photon imaging found that deep sleep increased the space between brain cells and improved the clearance of beta-amyloid, a protein linked to Alzheimer’s disease. Other research in Alzheimer’s model mice shows that chronic sleep restriction leads to higher buildup of beta-amyloid and tau over time.

Human studies report similar patterns. When sleep is disrupted or slow-wave sleep is reduced, levels of beta-amyloid in the cerebrospinal fluid can rise, and brain scans may show stronger amyloid signals. Because amyloid buildup is a core feature of Alzheimer’s disease, these findings suggest that long-term sleep problems could contribute to dementia risk. However, these studies show associations and mechanisms, not direct proof that poor sleep alone causes Alzheimer’s.

Improving sleep quality is often associated with better cognitive function and may lessen some risk factors linked with cognitive decline. In some studies, melatonin supplementation has been used as one tool to explore whether adjusting sleep-wake cycles can improve sleep parameters in specific groups with sleep disorders. These results cannot be generalized to everyone, and they do not prove that melatonin use prevents dementia, but they do support further research on sleep and long-term brain health.

Many studies and clinical guidelines describe melatonin as generally safe for short-term use in healthy adults at typical doses, although individual responses vary. For older adults and people with dementia or cognitive impairment, experts usually recommend additional caution and medical supervision.

Research in older adults with mild cognitive impairment or dementia-related sleep problems has explored melatonin as one of several options for addressing sleep difficulties.

In these studies, melatonin supplementation has been associated with:

• Changes in sleep timing when natural melatonin production appears low

• Reduced sundowning symptoms in some dementia patients during late afternoon or evening

• Measured improvements in specific sleep quality outcomes in certain dementia patients

• Shifts in disrupted circadian rhythms in some people with Alzheimer’s disease

These findings apply only to the dementia patients and older adults included in each study and should not be taken as proof that melatonin treatment will help all people with dementia sleep problems.

Studies and clinical reports note that older adults may be more likely to experience certain adverse effects from melatonin, especially at higher doses or when combined with sleep medications or other drugs that affect the central nervous system.

Reported side effects include:

• Daytime drowsiness or daytime drowsiness that lasts longer than expected

• Vivid dreams or changes in dream patterns

• Morning confusion, especially in frail older adults

• A higher risk of falls in some dementia patients

• Headaches or dizziness in some users

• Potential interactions with sleep medications, antidepressants, or other prescription drugs

These adverse effects have been observed in specific groups and doses studied and may not occur in every person taking melatonin, but they highlight the need for individualized medical advice.

Because of possible adverse events and drug interactions, many experts advise that certain people speak with a healthcare professional before taking melatonin.

This often includes people who:

• Take antidepressants, sleep medications, or other drugs that affect brain activity

• Have neurological disorders or a history of traumatic brain injury

• Have obstructive sleep apnea or other sleep disorders

• Take medications that increase sedation or dizziness

• Have existing balance problems or a high risk of falls

• Have questions about adverse effects, melatonin dosage, or long-term use

A healthcare professional can help weigh the potential risks and benefits of melatonin treatment in the context of each person’s medical history and sleep issues.

Researchers have studied melatonin in people with dementia to see whether it might play a role in dementia sleep management, but results are mixed. Dementia often disrupts circadian rhythms and sleep-wake cycles, and people with Alzheimer’s disease commonly report severe sleep problems.

Some small clinical trials and observational studies report that melatonin supplementation was associated with less agitation or fewer sundowning symptoms in certain groups of dementia patients. In these studies, some participants also showed improved sleep length or higher sleep quality scores. Other studies, however, did not find meaningful improvements compared with placebo. Because of differences in study design, disease severity, melatonin levels, and melatonin dosage, the findings cannot be generalized to all people with dementia.

Studies on circadian rhythms and circadian processes show that light exposure and evening routines influence melatonin production and sleep timing. Research on sleep hygiene suggests that dimming lights, limiting screen exposure, and using calm routines may support the body’s natural sleep-wake cycles. When melatonin supplementation is used in these research settings, it is often combined with these non-pharmacological approaches rather than used alone.

Differences in dementia type, stage of cognitive impairment, baseline melatonin levels in cerebrospinal fluid, and other medical conditions all affect how individuals respond to melatonin therapy. For this reason, study findings about improved sleep or sundowning symptoms apply only to the populations examined and do not guarantee that melatonin will work the same way for every person with dementia.

any experts recommend that melatonin use be individualized, especially for older adults and people with existing health conditions. Dose, timing, and supplement quality can all influence the balance between potential benefits and adverse effects.

In clinical trials and sleep research, melatonin has often been given in low doses taken in the evening, usually a few hours before bedtime, to line up with natural sleep-wake cycles. The best melatonin dosage for an individual can depend on age, sleep issues, and other medications. Because of this, many clinicians advise discussing melatonin treatment with a healthcare professional rather than choosing a dose without guidance.

Most clinical trials evaluate melatonin for weeks or a few months. These studies generally describe melatonin as well-tolerated in the short term at low to moderate doses in healthy adults and some older adults. Long-term safety data beyond about six to eighteen months are limited, particularly in dementia patients, so routine long-term use is usually approached with caution and medical monitoring.

Studies examining melatonin supplements have found that the actual melatonin levels in some products differ from what is listed on the label. Because of this, researchers and professional groups often recommend choosing brands that participate in third-party testing or programs such as USP verification. These steps do not guarantee outcomes, but they may reduce the chance of inconsistent dosing or unexpected adverse events.

Researchers and clinical guidelines often highlight non-pharmacological approaches as the foundation for managing sleep disorders and supporting cognitive health, especially in older adults and people with dementia.

Studies suggest that morning sunlight and regular light exposure can help regulate circadian rhythms. Physical activity and stress management strategies, such as relaxation exercises, are frequently associated with fewer sleep disturbances and improvements in some sleep problems. These approaches are often recommended alongside or before sleep aids.

Research on nutrition and sleep has explored how nutrients like magnesium, omega-3 fatty acids, and tryptophan relate to sleep quality and cognitive health. Some studies have found associations between these nutrients and certain sleep or cognitive outcomes, but results vary, and supplements are not a guaranteed solution to sleep issues. A balanced eating pattern and adequate hydration remain general recommendations for overall health.

Large population studies suggest that cognitive engagement and social connection are linked with better cognitive performance over time. Activities such as reading, conversation, games, and hobbies have been associated with lower rates of cognitive decline in some observational research. These findings support the idea that non-pharmacological strategies can contribute to long-term cognitive health alongside attention to sleep quality.

Based on current human studies, there is no clear evidence that melatonin causes dementia, and research so far has not shown that melatonin treatment increases dementia risk in the general population. Some clinical trials and laboratory research are exploring how melatonin’s antioxidant properties, effects on reactive oxygen species, and links to circadian rhythms might relate to cognitive health, but these findings are still developing and do not prove prevention of Alzheimer’s disease or other neurodegenerative diseases.

For people considering melatonin, the safest approach is to view it as one possible tool within a broader plan that includes good sleep hygiene, non-pharmacological treatments, and guidance from a healthcare professional who understands their medical history, sleep disturbances, and risk factors.