Overview

Leqembi® (lecanemab) and Kisunla™ (donanemab) are anti-amyloid monoclonal antibodies for selected people with mild cognitive impairment or mild dementia due to Alzheimer’s disease and confirmed brain amyloid. They remove amyloid plaques and can modestly slow the average rate of cognitive and functional decline. These are disease-modifying treatments: their purpose is to slow how quickly Alzheimer’s disease worsens, not to make memory noticeably better right away. They are not cures, do not stop the disease, and do not restore abilities already lost.¹²³⁴

The most important treatment risk is amyloid-related imaging abnormalities (ARIA): brain swelling or fluid called ARIA-E, and small areas of bleeding or iron deposition called ARIA-H. ARIA is often found only on a scheduled MRI, but it can cause symptoms, seizures, stroke-like deficits, permanent disability, or death. Both current U.S. labels carry boxed warnings for ARIA.¹²

Important context: Leqembi and Kisunla were studied in different trials, with different dosing, sample sizes, MRI schedules, and follow-up. The percentages below are useful for informed discussion, but they are not a head-to-head comparison and cannot predict one person’s outcome.

Evidence cutoff: This guide reflects publicly available evidence and current U.S. prescribing information through July 12, 2026. The main Alzheimer’s Association International Conference begins July 12, 2026; results scheduled for presentation after this cutoff are not treated here as established evidence.

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Who May Be Considered for Treatment?

Treatment is generally considered only when all of the following are true:

• Symptoms are at the mild cognitive impairment or mild dementia stage, and Alzheimer’s disease is the most likely primary cause.
• Amyloid pathology has been confirmed with an accepted test, commonly amyloid PET or cerebrospinal fluid testing.
• A recent brain MRI does not show a bleeding pattern, severe vascular injury, or another finding that makes treatment unacceptably risky.
• The patient and care partner can complete infusions or injections, scheduled MRIs, symptom monitoring, and follow-up visits.
• The expected benefit, ARIA risk, treatment burden, cost, and the patient’s goals support treatment.

These medicines have not been shown to help when started in people without cognitive symptoms, in moderate or severe dementia, or when another disease is the main cause of impairment.¹²

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How Leqembi and Kisunla Differ

Both medicines remove amyloid, but they bind different forms of amyloid and use different treatment strategies. These distinctions help explain the dosing plans; they do not prove that one medicine is clinically superior for a particular patient.¹²²⁰²¹

What Benefit Has Been Demonstrated?

The evidence comes from randomized trials, longer-term extension studies, and experience in clinical practice. These sources answer different questions, and the randomized trials remain the strongest evidence that the medicines caused the observed difference in decline.

Results from the randomized trials

Both pivotal trials used the Clinical Dementia Rating-Sum of Boxes (CDR-SB), an 18-point measure combining cognition and daily function. Higher scores mean greater impairment.

These percentages do not mean that patients improved by 27% or 29%. Both treated and placebo groups worsened; the treated groups worsened somewhat less on average.³⁴

Putting the difference into time

“Time saved” does not mean extra life expectancy. It means that, on average, the treated group reached a similar level of measured worsening later than the comparison group. During the randomized trial periods, this worked out to roughly 5 to 6 months of time-equivalent slowing by about 18 months with either medicine.¹³¹⁴

Kisunla: what the 36-month data add

The peer-reviewed TRAILBLAZER-ALZ 2 follow-up tracked participants for about three years. Compared with a matched untreated group from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), participants who started donanemab earlier had 1.2 points less CDR-SB worsening at three years (95% confidence interval, 0.7 to 1.7 points less worsening). Starting earlier was also associated with a 27% lower risk of progressing to the next CDR-Global stage than starting after the 76-week placebo period. More than 75% of assessed participants reached amyloid clearance, and benefit remained evident in people who had completed the treatment course.¹⁰

Kisunla’s PET-Based Treatment-Completion Strategy

In the pivotal program, 47% (313 of 672) of treated participants met the trial’s PET-based completion criteria by 12 months, and 69% (429 of 620) met them by 18 months. Completion meant an amyloid level below 11 Centiloids on one scan, or 11 to less than 25 Centiloids on two consecutive scans. It did not mean that Alzheimer’s disease had been cured or that cognition had stopped changing.²¹⁶

The current Lilly HCP summary reports that 85% of participants in the long-term extension met the trial’s PET completion criteria within three years. The peer-reviewed extension reports amyloid clearance in more than 75% of participants who had an evaluable scan; the percentages are not identical because the analytic populations and denominators differ.¹⁰¹⁶

In a smaller subgroup of 323 participants who met the PET completion criteria by one year, the 36-month CDR-SB difference was 1.3 points in favor of early donanemab compared with matched ADNI data. This suggests that benefit may persist after active dosing ends, but the analysis had no continuing placebo group and is less certain than the original randomized trial.¹⁶

Amyloid can return after treatment stops. The long-term report estimated relatively slow reaccumulation—approximately 2.4 Centiloids per year—and the current label reports a similar median estimate of 2.80 Centiloids per year. There is not yet a validated universal schedule for repeat PET imaging, retreatment, or restarting Kisunla after amyloid reaccumulates.²¹⁰

Leqembi: what the 48-month data add

In the Clarity AD longer-term follow-up, 478 participants were still receiving lecanemab at four years. Average CDR-SB worsening was 1.75 points lower than matched ADNI data and 2.17 points lower than BioFINDER data at 48 months. A dedicated analysis translated these differences into 11.0 months versus ADNI and 13.1 months versus BioFINDER, reasonably summarized as about 12 months at four years. A separate analysis reported a 34% lower relative risk of progressing to the next disease stage compared with matched ADNI data. These are longer-term comparisons with matched untreated groups, not four years of continuing placebo-controlled treatment.¹¹¹²¹³

What the 10-Year Lecanemab Projections Mean

At CTAD 2025, Eisai and Biogen presented a model that combined longer-term Clarity AD follow-up, results from 16 monoclonal-antibody studies, and ADNI data to estimate how disease-stage timing might change over 10 years. The model estimated that continued lecanemab treatment could delay average progression:

These are projections, not outcomes observed over 10 years. They assume that the treatment effect continues and that the comparison groups remain similar over time. The larger estimates in patients who started with less amyloid are especially uncertain and should not be presented as an expected result for one person.¹⁷

What proportion stayed stable or remained in an earlier disease stage?

These percentages are useful, but the endpoints must be named precisely. “No worsening on CDR-SB,” “no move to the next stage,” and “remaining within early Alzheimer’s disease” are related but are not the same outcome. In particular, the published long-term reports do not provide one clean, directly comparable percentage for people who started in MCI and remained specifically in MCI with each medicine.

Limits of the Long-Term Estimates

The first 18 months provide the strongest evidence because treatment and placebo were compared directly. The three-year Kisunla and four-year Leqembi results are also clinically useful, but they are less certain because the later comparisons were not part of a continuing randomized placebo trial.

Kisunla dosing update: The main efficacy trial used the earlier titration schedule. In a smaller safety study, the current dosing schedule lowered ARIA-E through 52 weeks from 24.9% to 16.2%. The newer schedule produced similar amyloid lowering at 24 weeks, but it was not a second placebo-controlled trial of cognitive and functional benefit.²⁵

How the Treatments Are Given and Monitored

Leqembi maintenance note: After 18 months, continuing every-two-week IV treatment or considering monthly IV or weekly subcutaneous maintenance are label-authorized options. The label states that transition to the less frequent maintenance regimens is supported by pharmacokinetic and pharmacodynamic modeling and that data on their long-term clinical benefit remain limited.¹

Additional MRI and clinical assessment are needed whenever symptoms suggest ARIA or when a scheduled MRI shows a new abnormality. Expert recommendations may add another MRI for higher-risk patients, and treatment centers may use policies stricter than the minimum label schedule.¹²⁷⁸

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Infusion Reactions and Allergic Reactions

An infusion-related reaction is not automatically the same as a true allergy. It may involve immune activation during or after an infusion and can cause fever, chills, body aches, headache, nausea, vomiting, flushing, dizziness, blood-pressure changes, chest discomfort, reduced oxygen level, or shortness of breath.

Why the Kisunla rates differ: The 16% current-regimen figure and the 9% original-regimen figure came from separately conducted studies. The higher rate in Study 2 should not be interpreted as proof that the gentler titration itself caused more infusion reactions; trial populations, observation, and event ascertainment can differ across studies.²

Infusion teams may slow or stop the infusion and treat symptoms. Premedication may be used after a prior reaction. Serious hypersensitivity to either medicine is a contraindication to receiving that medicine again.¹²

What Exactly Is ARIA?

• ARIA-E means edema or sulcal effusion: temporary swelling or fluid visible on MRI.
• ARIA-H means hemosiderin deposition: new microhemorrhages or superficial siderosis, an iron-containing blood-breakdown product along the brain surface.

ARIA-E and ARIA-H can occur together, so their percentages should not be added. Some microbleeds and siderosis occur spontaneously in Alzheimer’s disease because amyloid can collect in vessel walls, a process called cerebral amyloid angiopathy. Anti-amyloid therapy raises the risk further in susceptible patients.¹²

ARIA-E often improves or resolves on follow-up MRI. ARIA-H is different: the active bleeding process may stabilize, but the iron deposit can remain visible. It is therefore misleading to say that every form of ARIA simply “goes away.”

Current ARIA Rates in Clinical Trials

Study context: Leqembi’s figures come from an 18-month placebo-controlled trial; placebo rates were 9% for any ARIA, 2% for ARIA-E, 9% for ARIA-H, and 0.1% for hemorrhage larger than 1 cm. The current Kisunla figures come from a smaller active-regimen study designed primarily to compare titration schedules, not from a new placebo-controlled efficacy trial. For the rare large-hemorrhage outcome, 1% in 212 current-regimen participants is statistically less stable than 0.5% in the larger 853-person original-regimen pivotal study; both should be understood as infrequent group estimates rather than precise personal probabilities. The two drug columns should not be used to declare one medicine safer for a particular patient.¹²⁵

When Does ARIA Usually Occur?

Risk is front-loaded but never becomes zero. Most Leqembi ARIA-E events occurred within the first seven doses, and the label calls for enhanced vigilance during the first 14 weeks. Most Kisunla ARIA-E events occurred within the first 24 weeks. ARIA can occur later, recur, or appear after a previously normal MRI.¹²

How Severe Was ARIA on MRI?

With Leqembi, severe radiographic ARIA-E occurred in 1%; severe ARIA-H microhemorrhage in 3%; and severe superficial siderosis in 0.4%. With the current Kisunla titration, severe radiographic ARIA-E was not observed among 212 participants through 12 months, while severe ARIA-H microhemorrhage occurred in 2% and severe superficial siderosis in 1%. The Kisunla sample is too small for “zero observed” to be interpreted as zero true risk.¹²

APOE ε4: The Strongest Established Genetic Risk Factor

APOE ε4 is a common inherited variant. Two copies – one from each parent – confer the highest ARIA risk. Both labels recommend APOE testing before treatment so the risk discussion can be more individualized. Testing also reveals inherited information relevant to relatives, so the implications should be discussed before testing.¹²

Leqembi: Genotype-Specific Risk in the 18-Month Trial

There are two useful ways to present Leqembi risk by genotype. The current U.S. label gives a compact summary of any ARIA, symptomatic ARIA-E, and serious ARIA. The CLARITY AD subgroup analysis provides a more detailed breakdown of ARIA-E and ARIA-H. Both views are shown because they answer different questions.¹³

Current U.S. label summary

The label uses rounded percentages. “Any ARIA” includes MRI-detected ARIA-E, ARIA-H, or both. These categories overlap and should not be added.

Detailed CLARITY AD subgroup breakdown

These detailed rates come from the CLARITY AD genotype subgroup analysis. “Symptomatic ARIA-E” is more specific than “any symptomatic ARIA.” ARIA-E and ARIA-H may occur in the same person, so their percentages must not be summed.³

Kisunla: Why the Current Genotype Numbers Need Context

The current Kisunla dosing schedule has the most relevant safety data, but the APOE groups were small. The percentages below estimate risk during the first year, and the exact risk is less certain when only a small number of people were studied.²⁵

Current modified titration

Only 21 people with two ε4 copies received the current dosing schedule. That group is too small to estimate the true symptomatic risk reliably.

Larger original study: a more cautious guide for two-copy risk

This larger study used an earlier dosing schedule, so it is not the exact event rate for current dosing. It is included because the larger groups give a more reliable picture of risk by APOE status.²

Baseline MRI Findings That Raise Risk

For both medicines, the presence of at least two microhemorrhages or at least one area of superficial siderosis at baseline was associated with greater ARIA risk. The pivotal trials excluded many patients with higher-risk imaging, including more than four microhemorrhages, prior hemorrhage larger than 1 cm, vasogenic edema, and other vascular lesions; the exact exclusions differed by trial. Kisunla’s pivotal trial also excluded more than one area of superficial siderosis and severe white-matter disease.¹²

This matters because label rates come from a screened population. A person with more extensive cerebral amyloid angiopathy, prior hemorrhage, substantial vascular disease, or inability to undergo the required MRI monitoring may face a different or unacceptable risk. Expert recommendations and local programs may be more conservative than the label.⁷⁸

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Antiplatelet Medicines (Including Aspirin), Anticoagulants, and Clot-Busting Treatment

Aspirin is an antiplatelet medicine. These medication categories are not all treated the same: one antiplatelet medicine may be compatible with treatment after individual review, while chronic therapeutic anticoagulation is a greater concern.

• A single antiplatelet medicine – most commonly low-dose aspirin – may be compatible with treatment after individual review. Most clinical-trial experience was with aspirin. Evidence is more limited for non-aspirin antiplatelet medicines and especially for two antiplatelet medicines taken together.¹²
• Therapeutic anticoagulation is a greater concern. In the Leqembi pivotal trial, hemorrhage larger than 1 cm occurred in 2 of 79 patients (2.5%) receiving an anticoagulant alone or with an antiplatelet, versus none in the placebo subgroup. The group was small, so the exact risk is uncertain.¹
• Many specialty programs do not offer anti-amyloid treatment to patients who require chronic therapeutic anticoagulation, such as warfarin, apixaban, rivaroxaban, dabigatran, edoxaban, or heparin. Clot-busting treatment for possible stroke also requires special caution because ARIA can look like a stroke.⁷⁸

Fatal hemorrhage after thrombolysis has occurred. The Kisunla label describes one fatal hemorrhage after a thrombolytic in the original-regimen study and one in the current modified-regimen study. In the longer-term lecanemab follow-up, two intracerebral-hemorrhage deaths occurred during lecanemab exposure: one after tPA and one in a patient receiving anticoagulation. These events are rare but real. They do not justify delaying a 911 call for possible stroke; they do make immediate disclosure of anti-amyloid treatment essential.¹²⁶

Do not start or stop aspirin, another antiplatelet medicine, an anticoagulant, or any other medicine that affects clotting on your own. The treating neurologist and the clinician who prescribed the medicine should make a coordinated decision.

Suggested Medical-Alert Wording

Symptoms That Need Prompt Evaluation

Contact the treatment team promptly for a new or worsening headache, confusion, unusual sleepiness, dizziness, imbalance, difficulty walking, visual change, nausea or vomiting, speech difficulty, weakness, numbness, seizure, or loss of awareness.

What Happens If ARIA Is Found?

Management depends on symptoms and MRI severity. Some people with mild, asymptomatic ARIA may continue treatment under label-directed clinical judgment and close MRI follow-up. Symptomatic, moderate, or severe ARIA usually leads to treatment suspension; severe or recurrent events may lead to permanent discontinuation. Follow-up MRI is used to confirm that ARIA-E has resolved and ARIA-H has stabilized before a restart is considered.¹²⁷⁸

The risk-benefit decision should be revisited after any ARIA event, any new need for anticoagulation, progression beyond the mild stage, repeated missed MRIs, or a change in the patient’s goals or treatment burden.

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An Unresolved MRI Question: Brain-Volume Change

Several anti-amyloid trials have reported greater MRI-measured loss of whole-brain or hippocampal volume, or greater ventricular enlargement, in treated groups than in placebo groups. The biological meaning is unsettled. Proposed explanations range from removal of plaque, fluid, and inflammation—sometimes called amyloid-removal-related pseudoatrophy—to the possibility that some of the change reflects treatment-related tissue injury.¹⁸¹⁹

These MRI volume changes are not the same as proven accelerated neuronal loss, have not been validated as a patient-level measure of harm, and are not currently used like ARIA to decide whether a scheduled dose should be given. They nevertheless deserve transparent reporting and further study. This unresolved research question does not replace the established MRI surveillance required for ARIA.¹⁸¹⁹

What Do Real-World Data Add?

Real-world evidence is now large enough to be useful, but it answers different questions from a randomized trial. It can show whether patients complete MRIs, receive doses on schedule, remain on therapy, and experience safety events in ordinary practice. It is much less reliable for proving cognitive benefit because there is usually no randomized untreated control.

A 2026 U.S. claims analysis included 10,763 people with continuous healthcare encounters after at least one IV lecanemab treatment. Dosing intervals were generally close to the recommended every-two-week schedule. In a smaller subgroup of 371 people with enough follow-up to estimate longer persistence, 78.4% remained on treatment at 18 months, 71.7% at 20 months, and 67.3% at 24 months. This supports real-world feasibility and willingness to continue, but claims data do not establish cognitive effectiveness or explain why an individual stopped.¹⁵

A preliminary 2026 ALZ-NET conference abstract described 742 people receiving commercial Leqembi for an average of 8.4 months. ARIA-E was reported in 5% and ARIA-H in 7%, with symptomatic events in about 1% for each category. These findings are reassuring but should not replace the label rates in consent discussions: follow-up was shorter than the pivotal trial, the data were preliminary, and the report was a conference abstract rather than a complete peer-reviewed analysis.⁹

Clinical context: Real-world experience increasingly shows that organized programs can deliver treatment and monitoring at scale. For effectiveness counseling, however, the randomized trials and long-term extension analyses remain more informative than a clinician’s impression that a patient appears “stable.”

Questions to Ask Before Starting

1. How certain are we that Alzheimer’s disease is the main cause of the symptoms and that I am still in the stage studied?
2. What does my baseline MRI show about microbleeds, superficial siderosis, white-matter disease, or prior hemorrhage?
3. What is my APOE ε4 result, and how does it change my personal risk?
4. Can aspirin or another single antiplatelet be continued, and does any anticoagulant make treatment too risky?
5. What is this program’s plan for anticoagulation, emergency clot-busting treatment, missed MRIs, recurrent ARIA, and restarting or stopping treatment?
6. How will we judge whether the modest potential benefit remains worth the medical risk, time, cost, and burden?
7. What should my care partner monitor, and whom should we call after hours?

Anti-amyloid therapy can modestly slow decline in carefully selected patients with early, amyloid-confirmed Alzheimer’s disease. The randomized trials correspond to about 5 to 6 months of average time-equivalent slowing by roughly 18 months. Longer follow-up is reasonably summarized as about seven months at three years with Kisunla and about 12 months at four years with Leqembi. These later estimates are useful but less certain because there was no continuing randomized placebo group. ARIA is common on MRI, symptoms occur in a small minority, and serious or fatal brain bleeding is rare but possible. Safe treatment requires accurate diagnosis and staging, APOE counseling, a high-quality baseline MRI, scheduled follow-up imaging, a care partner, rapid evaluation of new symptoms, and a clear plan for anticoagulation and emergency stroke care.

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References

1. U.S. National Library of Medicine. LEQEMBI (lecanemab-irmb) U.S. Prescribing Information. Label updated June 30, 2026; accessed July 11, 2026.
2. U.S. National Library of Medicine. KISUNLA (donanemab-azbt) U.S. Prescribing Information. Current label accessed July 11, 2026.
3. van Dyck CH, Swanson CJ, Aisen P, et al. Lecanemab in Early Alzheimer’s Disease. N Engl J Med. 2023;388:9-21. doi:10.1056/NEJMoa2212948. (Supplementary Appendix).
4. Sims JR, Zimmer JA, Evans CD, et al. Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial. JAMA. 2023;330(6):512-527. doi:10.1001/jama.2023.13239.
5. Wang H, Monkul Nery ES, Ardayfio P, et al. Modified titration of donanemab reduces ARIA risk and maintains amyloid reduction. Alzheimer’s & Dementia. 2025;21:e70062. doi:10.1002/alz.70062.
6. Honig LS, Barakos J, Dhadda S, et al. Updated safety results from phase 3 lecanemab study in early Alzheimer’s disease. Alzheimers Res Ther. 2024;16:105. doi:10.1186/s13195-024-01441-8.
7. Cummings J, Apostolova L, Rabinovici GD, et al. Lecanemab: Appropriate Use Recommendations. J Prev Alzheimers Dis. 2023;10(3):362-377. doi:10.14283/jpad.2023.30.
8. Rabinovici GD, Selkoe DJ, Schindler SE, et al. Donanemab: Appropriate use recommendations. J Prev Alzheimers Dis. 2025;12(5):100150. doi:10.1016/j.tjpad.2025.100150.
9. Sabbagh M, et al. Commercial Lecanemab Safety Surveillance in the ALZ-NET Registry. American Academy of Neurology Annual Meeting abstract. 2026. Preliminary conference abstract; not yet a full peer-reviewed report.
10. Zimmer JA, Sims JR, Evans CD, et al. Donanemab in early symptomatic Alzheimer’s disease: results from the TRAILBLAZER-ALZ 2 long-term extension. J Prev Alzheimers Dis. 2026;13(2):100446. doi:10.1016/j.tjpad.2025.100446.
11. Eisai Co., Ltd. and Biogen Inc. Early Alzheimer’s Patients Continue to Benefit from Four Years of LEQEMBI Therapy: New Clinical Data Presented at AAIC. July 30, 2025. Sponsor news release reporting the Clarity AD open-label-extension analysis.
12. van Dyck CH, et al. Clarity AD open-label extension: efficacy and disease-stage analyses through 48 months. AAIC 2025 presentation. Sponsor-supported conference material.
13. Dickson S, Whetten J, Hendrix S, et al. Long-Term Benefit of Lecanemab: Estimation of Time Saved Through 48 Months. CTAD 2025 poster. Sponsor-supported conference material.
14. Dickson SP, Wessels AM, Dowsett SA, et al. “Time Saved” as a Demonstration of Clinical Meaningfulness and Illustrated Using the Donanemab TRAILBLAZER-ALZ Study Findings. J Prev Alzheimers Dis. 2023;10(3):595-599. doi:10.14283/jpad.2023.50.
15. Eisai Co., Ltd. Results from Real-World, Long-Term Treatment Persistence with LEQEMBI in the United States Presented at AD/PD 2026. March 23, 2026. Sponsor news release describing a claims-based observational analysis.
16. Eli Lilly and Company. KISUNLA efficacy, disease-stage, treatment-completion, and long-term-extension data. HCP website summarizing TRAILBLAZER-ALZ 2 and exploratory long-term analyses; accessed July 11, 2026.
17. Eisai Co., Ltd. and Biogen Inc. Eisai Presents New Data on the Continued and Expanding Benefit of LEQEMBI Maintenance Treatment in Early Alzheimer’s Disease at CTAD 2025. December 4, 2025. Sponsor news release describing a 10-year modeled time-savings analysis.
18. Belder CRS, Boche D, Nicoll JAR, et al. Brain volume change following anti-amyloid β immunotherapy for Alzheimer’s disease: amyloid-removal-related pseudo-atrophy. Lancet Neurol. 2024;23(10):1025-1034. doi:10.1016/S1474-4422(24)00335-1.
19. Alves F, Ayton S. Missing tissue, missing data: Resolving brain volume loss caused by anti-amyloid therapies. PLoS Med. 2026;23:e1004880. doi:10.1371/journal.pmed.1004880.
20. AlzForum. Leqembi therapeutic profile. Development history and mechanism overview; accessed July 11, 2026.
21. AlzForum. Kisunla therapeutic profile. Development history and mechanism overview; accessed July 11, 2026.

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