The Medical Letter on Drugs and Therapeutics
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ISSUE
1751
March 30, 2026
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Drugs for Dementia
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Disclosures
Principal Faculty
  • Jean-Marie Pflomm, Pharm.D., Editor in Chief has disclosed no relevant financial relationships.
Additional Contributor(s)
  • Brinda M. Shah, Pharm.D., Consulting Editor has disclosed no relevant financial relationships.
Objective(s)
Upon completion of this activity, the participant will be able to:
  1. Explain the current approach to the management of Alzheimer's disease dementia and mild cognitive impairment.
  2. Discuss the drugs available for treatment of Alzheimer's disease dementia and other dementias and compare them based on their efficacy, dosage and administration, potential adverse effects, and drug interactions.
  3. Determine the most appropriate therapy given the clinical presentation of an individual patient with Alzheimer's disease dementia or mild cognitive impairment.
 Select a term to see related articles  aducanumab   Aduhelm   Alzheimer's disease   antidepressants   antipsychotics   apoaequorin   Aricept   Auvelity   benzgalantamine   brexpiprazole   bupropion   Celexa   citalopram   dementia   dextromethorphan   donanemab   donepezil   Ebixa   Elecsys   Exelon   galantamine   herbals   Kisunla   Lecanemab   Leqembi   Lumipulse   memantine   Namzaric   Nuedexta   Nuplazid   Parkinson's disease   pimavanserin   PrecivityAD   Prevagen   quetiapine   quinidine   Rexulti   rivastigmine   Seroquel   sertraline   Zoloft   Zunveyl 
Med Lett Drugs Ther. 2026 Mar 30;68(1751):49-56   doi:10.58347/tml.2026.1751a
Summary: Drugs for Dementia
  • Cholinesterase inhibitors (donepezil, galantamine, benzgalantamine, rivastigmine) can modestly improve symptoms of dementia in patients with Alzheimer’s disease (AD), but they do not stop or reverse cognitive decline or the underlying neurodegenerative processes. They are generally not recommended for treatment of mild cognitive impairment (MCI).
  • The NMDA receptor antagonist memantine may provide modest benefit in patients with moderate to severe AD dementia. It causes fewer adverse effects than cholinesterase inhibitors. Whether adding memantine to a cholinesterase inhibitor is more effective than a cholinesterase inhibitor alone remains to be established.
  • The amyloid beta-directed monoclonal antibodies donanemab and lecanemab can reduce amyloid beta plaques in the brain and modestly slow cognitive decline in patients with MCI or mild AD dementia, but they have not been shown to stop or reverse cognitive decline or the underlying neurodegenerative processes. They can cause amyloid-related imaging abnormalities (ARIA), including cerebral edema and microhemorrhages.
Outline Tables

Alzheimer's disease (AD) is the most common cause of dementia, but cognitive decline also occurs in other neurological conditions, such as Parkinson's disease, Lewy body dementia, vascular dementia, and frontotemporal dementia.

Mild cognitive impairment (MCI) is generally defined as cognitive decline that is greater than expected based on an individual's age and level of education, but does not interfere with daily function; it may be a transitional state between the cognitive changes of normal aging and dementia.1

CHOLINESTERASE INHIBITORS

The cholinesterase inhibitors donepezil, galantamine, benzgalantamine (a prodrug of galantamine), and rivastigmine are FDA-approved for treatment of AD dementia. Rivastigmine is also approved for treatment of dementia associated with Parkinson's disease. None of these drugs are approved for treatment of Lewy body dementia, vascular dementia, or frontotemporal dementia.

Cognitive decline in AD is associated with loss of nicotinic and muscarinic cholinergic receptors and depletion of acetylcholine, which is involved in learning and memory. Cholinesterase inhibitors increase acetylcholine concentrations in the brain. They can modestly improve cognition, psychological symptoms, and daily function in patients with AD dementia, but they do not stop or reverse cognitive decline or the underlying neurodegenerative processes.2 They are generally not recommended for treatment of MCI.3

Adverse Effects – Gastrointestinal (GI) adverse effects are common with use of cholinesterase inhibitors, especially during initial treatment. Bradycardia and syncope can occur rarely; an increased incidence of falls and hip fractures has been reported in older adults taking these drugs. Because of their cholinergic effects, cholinesterase inhibitors should be used with caution in patients who are at increased risk for peptic ulcer disease and/or GI bleeding and in those with asthma or chronic obstructive pulmonary disease (COPD).

Drug Interactions – Use of cholinesterase inhibitors with other drugs that have cholinergic effects can result in additive effects. Use with drugs that have anticholinergic properties can antagonize the effects of cholinesterase inhibitors.

View the Comparison Table: Drugs for Alzheimer's Disease Dementia

DONEPEZIL — Donepezil (Aricept, and generics), a reversible inhibitor of acetylcholinesterase, is FDA-approved for treatment of mild, moderate, or severe AD dementia.

Clinical Studies – AD – Donepezil has been shown to modestly improve cognition and global functioning in patients with all stages of AD dementia, including those with severe disease living in assisted-care facilities. It has not been shown to delay institutionalization or slow progression of disability.4,5

In a 24-week trial in patients with moderate to severe AD dementia, donepezil 23 mg/day was more effective in improving cognition than 10 mg/day but it caused more GI adverse effects.6

Other Dementias – Some small, short-term trials in patients with Parkinson's disease dementia, Lewy body dementia, or vascular dementia have found modest improvements in cognition, global functioning, and activities of daily living with donepezil.7,8

Adverse Effects – The most common adverse effects of donepezil are nausea, vomiting, diarrhea, anorexia, fatigue, and muscle cramps; these effects generally resolve with continued treatment. Sleep disturbances have been reported.

Drug Interactions – Donepezil is metabolized primarily by CYP2D6 and 3A4. Serum concentrations of the drug may be increased in patients who are CYP2D6 poor metabolizers or are taking a CYP2D6 or 3A4 inhibitor.9

GALANTAMINE — Galantamine is a reversible acetylcholinesterase inhibitor. It is also a positive allosteric modulator of nicotinic acetylcholine receptors. Galantamine and benzgalantamine (Zunveyl), a prodrug of galantamine, are FDA-approved for treatment of mild to moderate AD dementia.10

Clinical Studies – AD – In short-term (4-6 months) trials in patients with mild to moderate AD dementia, galantamine modestly improved cognitive and global functioning compared to placebo.11-13 In a 2-year trial in patients with mild to moderate AD dementia, galantamine was associated with less cognitive and functional impairment and lower mortality rates than placebo.14 Addition of galantamine did not improve cognition, mortality, or activities of daily living in the subset of patients taking the N-methyl-D-aspartate (NMDA) receptor antagonist memantine at randomization.15

In two trials (6-12 months) in patients with AD dementia and/or cerebrovascular disease, treatment with galantamine improved cognition, global functioning, behavior, and activities of daily living.16,17

Adverse Effects – Nausea, vomiting, diarrhea, dizziness, headache, and weight loss are common with rapid dose escalation of galantamine but are less common during maintenance treatment. Depression, fatigue, and somnolence have been reported.

Drug Interactions – Galantamine is a substrate of CYP3A4 and CYP2D6; coadministration of drugs that inhibit or induce these isozymes may alter serum concentrations of galantamine and its more potent active metabolite.9 Serum concentrations of galantamine may be higher in patients who are CYP2D6 poor metabolizers. Dose dumping could occur if benzgalantamine is taken with alcohol.

RIVASTIGMINE — Rivastigmine is a carbamate-based, slowly reversible acetylcholinesterase inhibitor. It is FDA-approved for treatment of mild to moderate dementia associated with AD or Parkinson's disease. The transdermal patch formulation (Exelon Patch, and generics) is also FDA-approved for treatment of severe AD dementia.

Clinical Studies – AD – In a review of 13 placebo-controlled trials (12-52 weeks) in patients with mild to moderate AD dementia, use of oral or transdermal rivastigmine was associated with a modestly slowed rate of cognitive decline and improved activities of daily living.18

In a 24-week trial in patients with Alzheimer's-type dementia, transdermal rivastigmine (9.5 mg/24 hours) was similar in efficacy to oral rivastigmine (12 mg/day), but the incidence of nausea and vomiting was lower with the patch.19 In a 24-week trial, patients with severe AD dementia were randomized to receive either 4.6 or 13.3 mg/24 hours of transdermal rivastigmine; mean decreases from baseline on assessments of cognition and overall function were statistically significantly smaller with the 13.3-mg patch.20

Other Dementias – In a small 24-week trial in patients with Parkinson's disease dementia, treatment with transdermal rivastigmine led to improvements in attention and cognition.21 In a small 20-week trial in patients with Lewy body dementia, use of oral rivastigmine resulted in improvements in behavior.22 A 24-week trial in patients with probable vascular dementia found that treatment with oral rivastigmine improved measures of cognition, but not global impression of change or activities of daily living.23

Adverse Effects – Oral rivastigmine commonly causes nausea, vomiting, and diarrhea; GI tolerability can be improved with slow titration and by taking the drug with food. GI adverse effects occur less frequently with the transdermal formulation.

CHOICE OF A CHOLINESTERASE INHIBITOR — Most studies of cholinesterase inhibitors have shown modest improvements in cognitive and functional measures in patients with AD dementia. The drugs appear to be similar in efficacy and safety, but comparative trials are lacking. A matched cohort study of 17,478 patients from the Swedish Dementia Registry found that use of any cholinesterase inhibitor was associated with a reduction in cognitive decline and a lower risk of death; galantamine was associated with lower rates of cognitive decline and mortality than donepezil and rivastigmine.24 Transdermal rivastigmine causes fewer GI adverse effects than the oral formulation. Both donepezil and rivastigmine have documented efficacy in Parkinson's disease dementia and Lewy body dementia. Donepezil, rivastigmine, and galantamine have improved cognitive performance in patients with vascular dementia.

AN NMDA RECEPTOR ANTAGONIST

MEMANTINE — The N-methyl-D-aspartate (NMDA) receptor antagonist memantine (Namenda, and generics) is FDA-approved for treatment of moderate to severe AD dementia. Its mechanism of action in AD is unclear; it may reduce glutamatergic overstimulation at the NMDA receptor.25 An extended-release, fixed-dose combination of memantine and donepezil (Namzaric) is FDA-approved for once-daily treatment of moderate to severe AD dementia.

Clinical Studies – AD – There is no acceptable evidence that memantine is effective in mild AD dementia.

A meta-analysis of 15 trials in patients with moderate to severe AD dementia found small but consistent improvements, compared to placebo, in cognitive function, activities of daily living, behavior, and mood.26

In a 24-week trial in patients with mild to moderate AD dementia taking a cholinesterase inhibitor, addition of memantine was no more effective than addition of placebo.27

In a trial in patients with moderate to severe AD dementia taking donepezil, addition of memantine led to improvements in cognition, behavior, activities of daily living, and global outcomes compared to addition of placebo.28 In another trial, however, addition of memantine in patients who had taken donepezil for ≥3 months did not provide a significant benefit.29

Other Dementias – Memantine has been reported to improve cognition in patients with mild to moderate vascular dementia.30,31 It has not been shown to be effective for treatment of Parkinson's disease dementia or Lewy body dementia.32

Adverse Effects – Memantine is usually well tolerated. Dizziness, headache, confusion, and constipation have been reported. Hallucinations and delusions can occur.

Drug Interactions – Memantine does not affect the activity of cholinesterase inhibitors. Amantadine, which is used to treat Parkinson's disease, is also an NMDA receptor antagonist; taking it with memantine could theoretically result in additive adverse effects.

AMYLOID BETA-DIRECTED ANTIBODIES

The IV amyloid beta-directed monoclonal antibodies donanemab (Kisunla) and lecanemab (Leqembi, Leqembi Iqlik) are FDA-approved for treatment of AD; they should only be initiated in patients with MCI or mild dementia after confirmation of brain amyloid pathology.33,34 No data are available on their safety or efficacy for moderate or severe AD dementia. Both drugs reduce amyloid beta plaques in the brain and modestly slow cognitive decline, but neither drug has been shown to stop or reverse cognitive decline or the underlying neurodegenerative processes. The amyloid beta-directed monoclonal antibody aducanumab (Aduhelm) was withdrawn from the market in 2024 for commercial reasons.

DONANEMAB — In a randomized trial in patients with brain amyloid and tau pathology and either MCI or mild AD dementia, patients treated with donanemab experienced less cognitive and functional decline than those who received placebo at 76 weeks. Donanemab-treated patients were switched to placebo at week 24 or 52 if the amyloid plaque level on PET imaging fell below a prespecified threshold that signified full clearing.35

LECANEMAB — In a randomized 18-month trial in patients with early AD (MCI or mild dementia), patients treated with lecanemab experienced less cognitive decline than those who received placebo. Reductions in brain amyloid were significantly greater with lecanemab than with placebo.36

View the Comparison Table: Amyloid Beta-Directed Antibodies for Alzheimer's Disease

Adverse Effects – Common adverse effects of donanemab and lecanemab include infusion-related reactions, headache, and amyloid-related imaging abnormalities (ARIA), including cerebral edema (ARIA-E), microhemorrhages (ARIA-H), and superficial siderosis. The labels of both drugs contain a boxed warning about the risk of ARIA associated with their use. The incidence of ARIA appears to be higher with donanemab than with lecanemab, but direct comparisons are lacking. Serial MRI screening for ARIA is recommended during treatment (see Table 2). Most cases of ARIA-E have been detected by scheduled MRIs in asymptomatic patients. The risk of ARIA is greater in patients who are APOE4 allele carriers, particularly homozygotes. Use of these drugs has been associated with accelerated whole brain volume loss; the clinical significance of this finding is unclear.

Drug Interactions – The risk of intracerebral hemorrhage is increased when either donanemab or lecanemab is used concomitantly with antithrombotic drugs.37

SUPPLEMENTS

In a randomized trial, patients with mild to moderate AD received 2000 IU/day of vitamin E, 20 mg/day of memantine, a combination of vitamin E and memantine, or placebo. Compared to placebo, functional decline was statistically significantly slower with vitamin E, but not with memantine or the combination.38 A long-term study of antioxidant supplements found that vitamin E did not prevent dementia.39

The dietary supplement Ginkgo biloba is heavily promoted for memory support. In several randomized, double-blind trials, it was not effective for treatment of dementia or for prevention of cognitive decline in older adults.40,41

The dietary supplement Prevagen, which contains a synthetic form of the protein apoaequorin, is heavily promoted to improve memory. There is no acceptable evidence that it is effective.42

DRUGS FOR BEHAVIOR AND AGITATION

ANTIPSYCHOTICS — Antipsychotic drugs are widely used off-label to treat agitation and other behavioral symptoms in elderly patients, especially those with dementia. Second-generation antipsychotic drugs such as quetiapine (Seroquel, and generics) are generally preferred over first-generation drugs because they are less likely to cause extrapyramidal effects.43

Efficacy – In one placebo-controlled, 36-week trial in outpatients with AD, treatment with an antipsychotic drug modestly improved behavioral symptoms such as anger, aggression, and paranoid ideation, but not functioning, care needs, or quality of life.44

The oral second-generation antipsychotic drug brexpiprazole (Rexulti) is FDA-approved for once-daily treatment of agitation associated with dementia due to AD. Brexpiprazole acts as a partial agonist at serotonin 5-HT1a and dopamine D2 receptors and as an antagonist at serotonin 5-HT2a receptors. In two clinical trials in patients with agitation due to AD dementia, brexpiprazole (2 or 3 mg daily) improved agitation more than placebo.45

Adverse Effects – Common adverse effects of oral second-generation antipsychotic drugs include somnolence, gait changes, and urinary incontinence. Extrapyramidal effects can occur. In one trial in patients with AD, patients taking an antipsychotic drug were more likely to experience cognitive decline than those taking placebo.46

PIMAVANSERIN — An antipsychotic drug with no clinically significant effects on dopaminergic, adrenergic, histaminic, or muscarinic receptors, pimavanserin (Nuplazid, and generics) is FDA-approved for treatment of hallucinations and delusions associated with Parkinson's disease. It is an inverse agonist and antagonist at serotonin 5-HT2A receptors. In a randomized discontinuation trial in patients with any dementia-related psychosis, those who responded to open-label treatment with pimavanserin (62%) had a lower risk of relapse with continuation of the drug than with substitution of placebo.47

Adverse Effects – Pimavanserin does not cause somnolence, gait changes, or extrapyramidal effects, but it does prolong the QT interval and should not be used in patients with hepatic or severe renal impairment or cardiac conduction defects.

Risk of Death – The FDA requires that all antipsychotic drug labels include a warning about an increased risk of death in elderly patients with dementia treated with antipsychotic drugs. In randomized trials, elderly patients with dementia taking second-generation antipsychotic drugs had a higher mortality rate than those taking placebo (4.5% vs 2.6% in a typical 10-week controlled trial); most of the deaths were attributed to cardiovascular or infectious causes.

ANTIDEPRESSANTS — Antidepressant drugs are used off-label to treat agitation and other behavioral symptoms in patients with dementia. A review of 9 trials in a total of 692 patients with dementia found that the selective serotonin reuptake inhibitors (SSRIs) sertraline (Zoloft, and generics) and citalopram (Celexa, and generics) improved agitation, but not other behavioral symptoms.48

DEXTROMETHORPHAN/QUINIDINE — A fixed-dose combination of dextromethorphan, an uncompetitive NMDA receptor antagonist and a sigma-1 receptor agonist, and quinidine (Nuedexta) is FDA-approved for treatment of pseudobulbar affect, which occurs in a range of neurological disorders. Quinidine is a strong CYP2D6 inhibitor; it increases serum concentrations of dextromethorphan. In a randomized, placebo-controlled trial in 194 patients with AD-related agitation, measures of agitation and aggression were modestly improved in those receiving the combination. Adverse effects were infrequent, but included dizziness, falls, diarrhea, and urinary tract infection.49

Dextromethorphan/Bupropion – A fixed-dose combination of dextromethorphan and a low dose of bupropion, a norepinephrine and dopamine reuptake inhibitor that increases the bioavailability of dextromethorphan by inhibiting CYP2D6, previously approved by the FDA as Auvelity for treatment of major depressive disorder, is under FDA review for treatment of agitation in patients with AD. The combination has improved agitation-related and disruptive behaviors and delayed the time to relapse of AD agitation in clinical trials.

BLOOD TESTS FOR AD

Standard tests for detection of brain amyloid pathology to aid in the diagnosis of AD include amyloid PET scans and CSF biomarker testing. Detection of molecular biomarkers in blood (e.g., amyloid beta, phosphorylated Tau [pTau]) has been shown to correlate with the presence of amyloid pathology in the brain. Two blood tests for molecular biomarkers have been cleared by the FDA: the Elecsys Phospho-Tau (181P) Plasma test can be used to rule out amyloid pathology and the Lumipulse G pTau217/β-Amyloid 1-42 Plasma Ratio test can detect amyloid pathology. Neither test is recommended for stand-alone use or screening.50,51 Other blood tests have been marketed directly to consumers; they are not approved by the FDA and should not be used outside of clinical trials or specialist clinics.52

View the Comparison Table: Drugs for Alzheimer's Disease Dementia
View the Comparison Table: Amyloid Beta-Directed Antibodies for Alzheimer's Disease

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