Memantine

What it is

Memantine is a small synthetic molecule, 1-amino-3,5-dimethyladamantane hydrochloride, taken by mouth as a tablet, capsule or oral solution. It is a white to off-white powder, slightly soluble in water, with a molecular weight of 215.76. It is licensed in the United States only for moderate to severe dementia of the Alzheimer's type.

What the research says

Across high-certainty evidence from around 3,700 participants, memantine produces a small benefit in moderate-to-severe Alzheimer's disease - about 3.11 points on a 100-point cognitive scale over six months - and the reviewers themselves note that effect sizes in this field may be smaller than the minimum clinically important difference. In mild Alzheimer's disease, where it is widely prescribed off-label in the United States, the evidence shows no benefit. The label states plainly that there is no evidence it prevents or slows neurodegeneration.

Evidence grade: Limited evidence.

How it works

Drug class: Uncompetitive (open-channel) NMDA glutamate receptor antagonist

Glutamate is the brain's main excitatory signalling chemical, and over-activation of one of its receptors, the NMDA receptor, is thought to contribute to Alzheimer's symptoms. Memantine sits loosely in the open NMDA receptor channel and blocks it, which is meant to damp that excess signalling without shutting down normal transmission. The label is explicit that this does not amount to slowing the disease. (Source 1)

What it is used for

• High-certainty Cochrane evidence from up to 14 studies in around 3,700 participants shows a small benefit: 3.11 points on the Severe Impairment Battery, 1.09 points on an activities-of-daily-living scale, 0.21 CIBIC+ points. The reviewers note these effects may be below the minimum clinically important difference. Evidence: limited. (Source 2)
• Cochrane found probably no difference from placebo on cognition, function or behaviour, and an increase in discontinuation for adverse events (RR 2.12). An independent meta-analysis of manufacturer data reached the same conclusion, calling the evidence for mild Alzheimer's lacking and that for moderate disease meager. Evidence: not-supported. (Source 3)
• Moderate-certainty evidence from three additional studies found memantine is not beneficial as a treatment for agitation, with a clinical benefit of 0.50 CMAI points (95% CI -3.71 to 4.71), although fewer people taking it reported agitation as an adverse event. Evidence: not-supported. (Source 4)
• Two studies in around 750 participants: probably a small cognitive benefit of 2.15 ADAS-Cog points (95% CI 1.05 to 3.25), but probably no difference in global rating and possibly none in activities of daily living. Evidence: limited. (Source 5)
• A 2026 meta-analysis of six RCTs (n=288) found no statistically significant symptom reduction versus placebo (pooled mean difference -3.74 Y-BOCS points, 95% CI -9.95 to 2.47) with very high heterogeneity. The authors say it is not supported for routine use in unselected OCD. Evidence: not-supported. (Source 6)
• Cochrane describes the evidence here as limited and mainly low- or very low-certainty, from small studies of 133 to 319 people. Evidence: unknown. (Source 7)

Interactions

• Anything that makes the urine alkaline, including sodium bicarbonate supplements, carbonic anhydrase inhibitors and diet (pharmacokinetic study): Memantine is cleared mostly unchanged by the kidney, and that clearance falls by about 80% when the urine is alkaline. Sodium bicarbonate, carbonic anhydrase inhibitors, and diet can all shift urine pH, so memantine can build up and side effects increase. (Source 8)
• Other NMDA receptor antagonists: amantadine, ketamine and dextromethorphan (label): Combining memantine with other drugs that block the same receptor has not been studied systematically; the label advises caution. Dextromethorphan is in many over-the-counter cough preparations. (Source 9)
• Food (pharmacokinetic study): No food interaction: memantine is absorbed the same way with or without a meal, and the label says it can be taken either way. (Source 10)
• Drugs metabolised by liver CYP450 enzymes (pharmacokinetic study): Memantine is largely excreted unchanged and the liver's CYP450 system does not play a significant role in its metabolism, so classic CYP-based interactions, including with grapefruit juice and St John's wort, are not expected on pharmacokinetic grounds. (Source 10)

Stopping it

• There is no trial evidence on stopping memantine. A 2021 Cochrane review of withdrawal trials found six trials of cholinesterase inhibitor withdrawal and one of withdrawing either donepezil or memantine, and no trial assessing withdrawal of memantine alone. (Source 11)
• The same review states the position bluntly in its conclusions, while advising caution because the related evidence on stopping cholinesterase inhibitors points to worse cognition and function. (Source 12)
• Memantine is not a drug of dependence and no withdrawal syndrome is described. The only restarting instruction in the label is practical: after several missed days, the dose may need to be restarted low and titrated up again. (Source 13)
• Cochrane also notes that whether any benefit persists past six months has not been established, because no long-duration trial in moderate-to-severe Alzheimer's disease has been done. (Source 14)

What goes wrong

Memantine raises the risk of dizziness and probably headache, but not of falls, and overall adverse event rates match placebo. (Source 15)

• Systematic review, Moderate certainty.
• Size: All trials combined (44 trials, almost 10,000 participants)
• Who: People with dementia of various causes.
• How long: Mostly six months.
• Result: Any adverse event RR 1.03 (95% CI 1.00 to 1.06); dizziness 6.1% vs 3.9%; headache 5.5% vs 4.3%; no difference in falls.
• Funding: Cochrane review.

there is moderate-certainty evidence that memantine is 1.6 times more likely than placebo to result in dizziness (6.1% versus 3.9%), low-certainty evidence of a 1.3-fold increased risk of headache (5.5% versus 4.3%), but high-certainty evidence of no difference in falls.

In mild Alzheimer's disease, memantine may roughly double the number of people stopping treatment because of adverse events - the one place the mild-disease evidence shows a difference, and it is a harm. (Source 3)

• Systematic review, Low certainty.
• Size: Up to four studies in around 600 participants.
• Who: People with mild Alzheimer's disease (MMSE 20 to 23)
• How long: Six months.
• Result: RR 2.12, 95% CI 1.03 to 4.39 for discontinuation because of adverse events.
• Funding: Cochrane review.

Memantine (compared with placebo) may increase the numbers of people discontinuing treatment because of adverse events (RR 2.12, 95% CI 1.03 to 4.39).

In the pooled placebo-controlled trials used for the label, dizziness, headache, confusion and constipation were each a couple of percentage points commoner on memantine than placebo. (Source 16)

• Randomized trial, Moderate certainty.
• Size: 1,862 dementia patients (940 memantine, 922 placebo) in eight double-blind placebo-controlled trials.
• Who: Patients with Alzheimer's disease or vascular dementia.
• How long: Up to 28 weeks.
• Result: Dizziness 7% vs 5%; headache 6% vs 3%; confusion 6% vs 5%; constipation 5% vs 3%; hypertension 4% vs 2%; hallucination 3% vs 2%.
• Funding: Manufacturer trials reported in the FDA label.

Central and Peripheral Nervous System Dizziness 5 7 Headache 3 6 Gastrointestinal System Constipation 3 5

Rare but serious harms reported after marketing include blood dyscrasias, hepatitis, pancreatitis, acute renal failure, Stevens-Johnson syndrome and suicidal ideation. (Source 17)

• Case series, Very low certainty.
• Size: Spontaneous reports from a population of uncertain size.
• Who: Post-approval users of memantine.
• How long: Post-approval.
• Result: Frequency cannot be reliably estimated and causality cannot always be established.
• Funding: Manufacturer label, FDA-approved labelling.

Blood and Lymphatic System Disorders -agranulocytosis, leukopenia (including neutropenia), pancytopenia, thrombocytopenia, thrombotic thrombocytopenic purpura.

What the evidence supports

In moderate-to-severe Alzheimer's disease memantine gives a small benefit on cognition, function, behaviour and global rating at six to seven months. (Source 2)

• Systematic review, High certainty.
• Size: Up to 14 studies in around 3,700 participants (44 trials, almost 10,000 participants in the whole review)
• Who: People with moderate-to-severe Alzheimer's disease, with or without a concomitant cholinesterase inhibitor.
• How long: Six to seven months.
• Result: Cognitive function 3.11 Severe Impairment Battery points (95% CI 2.42 to 3.92); ADL 1.09 ADL19 points (95% CI 0.62 to 1.64); behaviour and mood 1.84 NPI points (95% CI 1.05 to 2.76); global rating 0.21 CIBIC+ points (95% CI 0.14 to 0.30)
• Funding: Cochrane review; for nearly half the studies relevant data were obtained from unpublished sources.

High-certainty evidence from up to 14 studies in around 3700 participants consistently shows a small clinical benefit for memantine versus placebo: clinical global rating (CGR): 0.21 CIBIC+ points (95% confidence interval (CI) 0.14 to 0.30); cognitive function (CF): 3.11 Severe Impairment Battery (SIB) points (95% CI 2.42 to 3.92)

What the evidence does not support

In mild Alzheimer's disease memantine is probably no different from placebo on cognition, daily function or behaviour. (Source 3)

• Systematic review, Moderate certainty.
• Size: Up to four studies in around 600 participants, from post-hoc subgroups.
• Who: People with mild Alzheimer's disease (MMSE 20 to 23)
• How long: Six months.
• Result: Cognition 0.21 ADAS-Cog points (95% CI -0.95 to 1.38); ADL -0.07 ADL 23 points (95% CI -1.80 to 1.66); behaviour -0.29 NPI points (95% CI -2.16 to 1.58); CGR 0.09 CIBIC+ points (95% CI -0.12 to 0.30)
• Funding: Cochrane review; based on post-hoc subgroups, which the review flags.

2. Mild AD (Mini Mental State Examination (MMSE) 20 to 23): mainly moderate-certainty evidence based on post-hoc subgroups from up to four studies in around 600 participants suggests there is probably no difference between memantine and placebo for CF: 0.21 ADAS-Cog points (95% CI -0.95 to 1.38)

An independent re-analysis of manufacturer trial data found no significant difference from placebo on any outcome in mild Alzheimer's disease, and only small differences in moderate disease. (Source 18)

• Meta-analysis, Moderate certainty.
• Size: 431 patients with mild AD and 697 with moderate AD across three trials.
• Who: Patients with mild (MMSE 20-23) or moderate (MMSE 10-19) Alzheimer's disease.
• How long: Trial durations as published, typically 24 weeks.
• Result: Mild AD: ADAS-cog -0.17 (95% CI -1.60 to 1.26), CIBIC-plus -0.09 (95% CI -0.30 to 0.12), ADCS-ADL 0.62 (95% CI -1.64 to 2.71), NPI 0.09 (95% CI -2.11 to 2.29). Moderate AD: ADAS-cog -1.33 (95% CI -2.28 to -0.38)
• Funding: Independent re-analysis of manufacturer-sponsored meta-analyses, registries and presentations.

Limit of this finding: One number in this sentence is not centred on its own confidence interval. The daily-living result is printed as "0.62 (95% CI, -1.64 to 2.71)", whose midpoint is 0.535, while the other three estimates in the same sentence sit exactly in the middle of theirs. One of the printed figures is therefore slightly wrong, most likely a typesetting slip. The quote reproduces the paper as printed. It does not change what the finding shows, because the interval crosses zero on any reading and the authors report no significant difference on any outcome in mild Alzheimer's disease; do not treat 0.62 as a precisely established value.

There were no significant differences between memantine and placebo on any outcome for patients with mild AD, either within any trial or when data were combined

The same authors concluded that evidence for memantine in mild Alzheimer's disease is lacking despite frequent off-label use, and that evidence in moderate disease is meager. (Source 19)

• Meta-analysis, Moderate certainty.
• Size: Three trials, 1,128 patients.
• Who: Patients with mild to moderate Alzheimer's disease.
• How long: As published.
• Result: No significant differences in mild AD; small differences on ADAS-cog and CIBIC-plus only in moderate AD.
• Funding: Independent re-analysis.

Despite its frequent off-label use, evidence is lacking for a benefit of memantine in mild AD, and there is meager evidence for its efficacy in moderate AD.

Memantine is not effective as a treatment for agitation in Alzheimer's disease. (Source 4)

• Systematic review, Moderate certainty.
• Size: Three additional studies beyond the main efficacy pool.
• Who: People with Alzheimer's disease and agitation.
• How long: Six months.
• Result: Clinical benefit of 0.50 CMAI points, 95% CI -3.71 to 4.71.
• Funding: Cochrane review.

there is also moderate-certainty evidence, from three additional studies, suggesting that memantine is not beneficial as a treatment for agitation (e.g. Cohen Mansfield Agitation Inventory: clinical benefit of 0.50 CMAI points, 95% CI -3.71 to 4.71)

Adjunctive memantine did not significantly reduce obsessive-compulsive symptoms versus placebo in a 2026 meta-analysis. (Source 6)

• Meta-analysis, Low certainty.
• Size: Six RCTs, 288 participants.
• Who: Adults with obsessive-compulsive disorder on established treatment.
• How long: 8 to 16 weeks, memantine 5-20 mg/day.
• Result: Pooled mean difference -3.74 Y-BOCS points, 95% CI -9.95 to 2.47, I2 = 97.9%; responder RR 3.62, 95% CI 0.16-80.71.
• Funding: Not stated in the abstract; PROSPERO CRD420251147106, GRADE and RoB 2 applied.

Overall, memantine did not produce a statistically significant symptom reduction versus placebo (pooled mean difference -3.74 points, 95% confidence interval [CI] -9.95 to 2.47), with high heterogeneity (I2 = 97.9%).

Memantine is not disease-modifying: the label states there is no evidence it prevents or slows neurodegeneration. (Source 1)

• Official position, Certainty not rated.
• Size: Not applicable.
• Who: Patients with Alzheimer's disease.
• How long: Not applicable.
• Result: No claim of disease modification is supported.
• Funding: Manufacturer label, FDA-approved labelling.

There is no evidence that memantine prevents or slows neurodegeneration in patients with Alzheimer’s disease.

Where the evidence is mixed

The reviewers themselves say the effect size may be less than the minimum clinically important difference. (Source 14)

• Systematic review, High certainty.
• Size: 44 trials, almost 10,000 participants.
• Who: People with dementia of various causes and severities.
• How long: Mostly six months.
• Result: Benefit in moderate-to-severe disease irrespective of concomitant cholinesterase inhibitor; no benefit in mild disease.
• Funding: Cochrane review.

Clinical heterogeneity in AD makes it unlikely that any single drug will have a large effect size, and means that the optimal drug treatment may involve multiple drugs, each having an effect size that may be less than the minimum clinically important difference.

Discontinuation for adverse reactions was no commoner on memantine than placebo in the label's pooled trials. (Source 20)

• Randomized trial, Moderate certainty.
• Size: 1,862 dementia patients across eight trials.
• Who: Patients with dementia receiving up to 20 mg/day.
• How long: Up to 28 weeks.
• Result: Discontinuation because of an adverse reaction 10.1% on memantine vs 11.5% on placebo.
• Funding: Manufacturer trials reported in the FDA label.

Limit of this finding: The label calls these two figures "the same", and they are not identical: 10.1 percent of people on memantine stopped because of an adverse reaction against 11.5 percent on placebo. The label gives no confidence interval and no p-value for the comparison, so it offers no way to tell whether that 1.4-point gap is chance. Read this as no signal that memantine made more people stop than placebo did, not as proof that the two rates are equal.

the likelihood of discontinuation because of an adverse reaction was the same in the memantine hydrochloride group (10.1%) as in the placebo group (11.5%)

Where the research disagrees

Whether memantine has any useful effect in mild Alzheimer's disease, where it is commonly prescribed off-label in the United States

• Cochrane Dementia and Cognitive Improvement Group (McShane and colleagues, 2019), systematic review of 44 trials: There is a small clinical benefit of memantine in people with moderate-to-severe AD, which occurs irrespective of whether they are also taking a ChEI, but no benefit in people with mild AD. (Source 14)
• Schneider and colleagues, re-analysing manufacturer data (2011), meta-analysis of manufacturer-sponsored trials: Despite its frequent off-label use, evidence is lacking for a benefit of memantine in mild AD, and there is meager evidence for its efficacy in moderate AD. (Source 19)
• The US FDA-approved label, as a regulatory position, regulatory position, label version dated 2026: Memantine hydrochloride tablets are indicated for the treatment of moderate to severe dementia of the Alzheimer’s type. (Source 21)

How much

• Reference intake: Dosing is set by the prescriber. As a position, section 2 Dosage and Administration of the FDA-approved memantine hydrochloride tablet label (Major Pharmaceuticals, label version dated 2026) states a starting dose of 5 mg once daily, increased in 5 mg steps at intervals of at least one week to a maintenance dose of 10 mg twice daily. (Source 13)
• Upper limit: Section 2 of the label states a maintenance dose, and the dose shown effective in controlled trials, of 20 mg/day; for severe renal impairment (creatinine clearance 5 to 29 mL/min) the label's target is 5 mg twice daily. (Source 13)
• Studied: Cochrane restricted its analyses to the licensed dose, 20 mg/day or 28 mg extended release, at six to seven months of follow-up. (Source 22)
• Studied: The label's safety database comes from eight double-blind placebo-controlled trials in 1,862 dementia patients at doses up to 20 mg/day for up to 28 weeks. (Source 20)
• Studied: The OCD trials used 5-20 mg/day over 8 to 16 weeks in 288 adults. (Source 6)

A common belief, and what the research shows

The belief: Memantine treats Alzheimer's disease, so starting it early will slow the illness down.

What the research shows: Neither claim is supported. The label itself says "There is no evidence that memantine prevents or slows neurodegeneration in patients with Alzheimer’s disease." And Cochrane, having looked at post-hoc subgroups from four trials in around 600 people with mild disease, wrote: "A definitive long-duration trial in mild AD is needed to establish whether starting memantine earlier would be beneficial over the long term and safe: at present the evidence is against this, despite it being common practice." In moderate-to-severe disease the benefit that does exist is small - 3.11 points on the Severe Impairment Battery.

Questions and answers

What is it?

Memantine is a synthetic small molecule, 1-amino-3,5-dimethyladamantane hydrochloride, taken by mouth. It is a white to off-white powder that is only slightly soluble in water, supplied as 5 mg and 10 mg film-coated tablets as well as capsules and a solution. It belongs to a different class from the older Alzheimer's drugs such as donepezil. (Source 23)

What does it do in the body?

It blocks the NMDA receptor, one of the receptors for glutamate, the brain's main excitatory signalling chemical. The theory is that persistent over-activation of this receptor contributes to Alzheimer's symptoms, and that loosely blocking the open channel damps that down. The label states directly that this does not amount to preventing or slowing nerve cell loss. (Source 1)

Is it good or bad for you?

It depends on the stage of disease. In moderate-to-severe Alzheimer's the benefit is real but small - 3.11 points on the Severe Impairment Battery, 1.09 points on a daily-living scale - and the reviewers warn it may be below what counts as clinically important. In mild Alzheimer's the evidence shows no benefit at all, and the one difference from placebo is more people stopping because of side effects. Tolerability overall is good: dizziness 6.1% versus 3.9% and no excess of falls. (Source 14)

How do you get more of it?

Memantine is a prescription medicine, not a nutrient, so the only way to have more of it is a prescriber changing the dose. As a position, the label describes starting at 5 mg once daily and increasing in 5 mg steps no faster than weekly to 10 mg twice daily, which is the dose shown effective in controlled trials. It can be taken with or without food. (Source 13)

If it is harmful, what reduces it?

Memantine is cleared mainly by the kidneys, unchanged, with a long half-life of about 60 to 80 hours - so it takes several days to wash out. Because clearance drops by about 80% when the urine is alkaline, anything that alkalinises urine, including sodium bicarbonate, slows elimination and raises levels. There is no antidote; the label's overdose management is supportive. (Source 10)

Why might someone be low in it or missing it?

Someone may not be on memantine because their dementia is mild, where the evidence does not support it, or is not Alzheimer's type, or because they stopped it. In the label's pooled trials 10.1% of people on memantine discontinued because of an adverse reaction, which was no more than the 11.5% on placebo. In mild Alzheimer's disease, by contrast, memantine may about double discontinuation for adverse events. (Source 3)

Which whole foods contain it or feed it?

No whole food contains memantine; it is a synthetic drug. Food does not affect how it is absorbed, so it can be taken with or without a meal. What does matter is anything that shifts urine pH towards alkaline - the label names diet among the things that alter urine pH, alongside drugs such as sodium bicarbonate. (Source 13)

What happens if you do not have it?

For someone with mild Alzheimer's disease, the evidence says essentially nothing changes - cognition, daily function and behaviour were no different from placebo. For someone with moderate-to-severe disease, going without means forgoing a small average benefit of around 3 points on a cognitive scale over six months. There is no trial evidence at all on what happens when memantine is stopped. (Source 12)

How can you test for it?

There is no blood test for memantine levels in routine care, and no biological test of whether it is working. What the trials measured are rating scales: the Severe Impairment Battery and ADAS-Cog for cognition, CIBIC+ for a clinician's global impression, ADL scales for daily function and the Neuropsychiatric Inventory for behaviour. These are observer-rated instruments, which is why Cochrane reports benefit in scale points rather than in anything measurable in blood. (Source 2)

References

1. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 12.1 Mechanism of Action. 2026. Read the source
2. Cochrane Database of Systematic Reviews. Memantine for dementia.. 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
3. Cochrane Database of Systematic Reviews. Memantine for dementia. (Mild Alzheimer disease subgroup). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
4. Cochrane Database of Systematic Reviews. Memantine for dementia. (Agitation). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
5. Cochrane Database of Systematic Reviews. Memantine for dementia. (Vascular dementia). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
6. CNS Drugs. Memantine Augmentation in Obsessive-Compulsive Disorder: A Systematic Review and Meta-analysis.. 2026. PMID 42484816, DOI 10.1007/s40263-026-01318-4. Read the source
7. Cochrane Database of Systematic Reviews. Memantine for dementia. (Other dementias). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
8. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 7.1 Drugs that Make the Urine Alkaline. 2026. Read the source
9. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 7.2 Use with Other N-methyl-D-aspartate (NMDA) Antagonists. 2026. Read the source
10. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 12.3 Pharmacokinetics. 2026. Read the source
11. Cochrane Database of Systematic Reviews. Withdrawal or continuation of cholinesterase inhibitors or memantine or both, in people with dementia. (Main results). 2021. PMID 35608903, DOI 10.1002/14651858.CD009081.pub2. Read the source
12. Cochrane Database of Systematic Reviews. Withdrawal or continuation of cholinesterase inhibitors or memantine or both, in people with dementia. (Authors’ conclusions). 2021. PMID 35608903, DOI 10.1002/14651858.CD009081.pub2. Read the source
13. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 2 Dosage and Administration. 2026. Read the source
14. Cochrane Database of Systematic Reviews. Memantine for dementia. (Authors’ conclusions). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
15. Cochrane Database of Systematic Reviews. Memantine for dementia. (Adverse events). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
16. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 6.1 Clinical Trials Experience (Table 1 and seizures). 2026. Read the source
17. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 6.2 Postmarketing Experience. 2026. Read the source
18. Archives of Neurology. Lack of evidence for the efficacy of memantine in mild Alzheimer disease.. 2011. PMID 21482915, DOI 10.1001/archneurol.2011.69. Read the source
19. Archives of Neurology. Lack of evidence for the efficacy of memantine in mild Alzheimer disease. (Conclusions). 2011. PMID 21482915, DOI 10.1001/archneurol.2011.69. Read the source
20. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 6.1 Clinical Trials Experience. 2026. Read the source
21. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 1 Indications and Usage. 2026. Read the source
22. Cochrane Database of Systematic Reviews. Memantine for dementia. (Data collection and analysis). 2019. PMID 30891742, DOI 10.1002/14651858.CD003154.pub6. Read the source
23. Major Pharmaceuticals / DailyMed (U.S. National Library of Medicine). MEMANTINE HYDROCHLORIDE tablet, film coated - Full Prescribing Information, section 11 Description. 2026. Read the source