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Lecanemab in early Alzheimer's disease
Open accessAbstract
BACKGROUND: The accumulation of soluble and insoluble aggregated amyloid-beta (Aβ) may initiate or potentiate pathologic processes in Alzheimer's disease. Lecanemab, a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils, is being tested in persons with early Alzheimer's disease. METHODS: We conducted an 18-month, multicenter, double-blind, phase 3 trial involving persons 50 to 90 years of age with early Alzheimer's disease (mild cognitive impairment or mild dementia due to Alzheimer's disease) with evidence of amyloid on positron-emission tomography (PET) or by cerebrospinal fluid testing. Participants were randomly assigned in a 1:1 ratio to receive intravenous lecanemab (10 mg per kilogram of body weight every 2 weeks) or placebo. The primary end point was the change from baseline at 18 months in the score on the Clinical Dementia Rating-Sum of Boxes (CDR-SB; range, 0 to 18, with higher scores indicating greater impairment). Key secondary end points were the change in amyloid burden on PET, the score on the 14-item cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog14; range, 0 to 90; higher scores indicate greater impairment), the Alzheimer's Disease Composite Score (ADCOMS; range, 0 to 1.97; higher scores indicate greater impairment), and the score on the Alzheimer's Disease Cooperative Study-Activities of Daily Living Scale for Mild Cognitive Impairment (ADCS-MCI-ADL; range, 0 to 53; lower scores indicate greater impairment). RESULTS: A total of 1795 participants were enrolled, with 898 assigned to receive lecanemab and 897 to receive placebo. The mean CDR-SB score at baseline was approximately 3.2 in both groups. The adjusted least-squares mean change from baseline at 18 months was 1.21 with lecanemab and 1.66 with placebo (difference, -0.45; 95% confidence interval [CI], -0.67 to -0.23; P<0.001). In a substudy involving 698 participants, there were greater reductions in brain amyloid burden with lecanemab than with placebo (difference, -59.1 centiloids; 95% CI, -62.6 to -55.6). Other mean differences between the two groups in the change from baseline favoring lecanemab were as follows: for the ADAS-cog14 score, -1.44 (95% CI, -2.27 to -0.61; P<0.001); for the ADCOMS, -0.050 (95% CI, -0.074 to -0.027; P<0.001); and for the ADCS-MCI-ADL score, 2.0 (95% CI, 1.2 to 2.8; P<0.001). Lecanemab resulted in infusion-related reactions in 26.4% of the participants and amyloid-related imaging abnormalities with edema or effusions in 12.6%. CONCLUSIONS: Lecanemab reduced markers of amyloid in early Alzheimer's disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events. Longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer's disease. (Funded by Eisai and Biogen; Clarity AD ClinicalTrials.gov number, NCT03887455.).
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“Phase 2 and phase 3 trials of the monoclonal antibodies -- aducanumab, lecanemab, and donanemab, as well as the discontinued gantenerumab -that target Aβ plaques, fibrils, soluble protofibrils, and oligomeric Aβ species all required PET or CSF evidence of amyloid pathology for trial enrolment. (460-463)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [460]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Adding the anti-amyloid therapy to ChEI treatment in early-stage AD, the cognitive function can be maintained better and longer in the years to come (5-10 years).10”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The advent of anti-amyloid immunotherapy, including the US Food & Drug Administration (FDA)-approved monoclonal antibodies such as lecanemab and donanemab, has proven efficacy in slowing cognitive decline in early-stage AD.”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The FDA approved two anti-amyloid immunotherapies, lecanemab and donanemab, for “early-stage” AD, encompassing both stage 3 (MCI) and stage 4 (mild dementia).”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Anti-amyloid immunotherapy with lecanemab or donanemab is now considered as an add-on therapy.10,20”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [10]
Experimental — accuracy not yet measured
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In the citing paper
“Recently, lecanemab received traditional approval from the US Food & Drug Administration (FDA) for treatment of patients with MCI and mild dementia with biomarker-proven Aβ pathology8”
From Highly accurate blood test for Alzheimer's disease is similar or superior to clinical cerebrospinal fluid tests (2024) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Several phase 3 trials demonstrated that anti-amyloid antibodies can clear Aβ plaques from the brain6–8, which leads to a slowing of cognitive and functional decline in individuals with mild cognitive impairment (MCI) and mild dementia due to AD.”
From Highly accurate blood test for Alzheimer's disease is similar or superior to clinical cerebrospinal fluid tests (2024) · cites this paper as [8]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For example, although patients with early-stage AD may be candidates for anti-amyloid therapies15–17, the coexistence of pathology from other etiologies, such as VD, can increase the risk of amyloid-related imaging abnormalities18.”
From AI-based differential diagnosis of dementia etiologies on multimodal data (2024) · cites this paper as [17]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Accumulation of amyloid beta (Aβ) is an early critical hallmark of the disease and thus is an important target for understanding pathophysiology and therapy.”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [1]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Current FDA-approved treatments, including cholinesterase inhibitors, memantine, and anti-amyloid monoclonal antibodies, offer modest symptomatic benefit or partial slowing of progression but do not halt neurodegeneration or restore lost neuronal circuits.”
From Reverse the progression of Alzheimer’s disease through Nano-ERASER-based adult neuroregeneration (2026) · cites this paper as [3]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Recent therapies targeting Aβ clearance using anti-Aβ monoclonal antibodies (mabs) during the early stages of AD provide minimal cognitive benefit”
From Perineuronal net deglycosylation associates with tauopathy‐induced gliosis and neurodegeneration (2024) · cites this paper as van Dyck et al. 2023
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“More recently, lecanemab (approved in 2023) and donanemab (approved in 2024) have demonstrated the ability to clear A β plaque deposits and slow cognitive decline by 25 to 30%”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Three anti-amyloid monoclonal antibodies aducanumab, lecanemab, and donanemab have demonstrated robust amyloid clearance, with statistically significant but modest clinical effects”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“although the FDA-approved anti-Aβ monoclonal antibodies are very effective at removing Aβ from the brain parenchyma, a substantial proportion of treated individuals, especially APOEε4 carriers, exhibit amyloid-related imaging abnormalities (ARIA) consisting of oedema (ARIA-E) and haemosiderin deposits (ARIA-H)2.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [2]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“ε4 carriers, particularly ε4 homozygotes, exhibit a substantially increased risk of amyloid-related imaging abnormalities (ARIA) during treatment with anti-amyloid monoclonal antibodies [2, 5, 8].”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Accordingly, ApoE genotyping is now increasingly considered an important component of the pre-treatment work-up for anti-amyloid therapies [5, 8, 11, 12].”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [5]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Current “disease- modifying” FDA-approved therapies for Alzheimer’s are anti-amyloid antibody drugs, which successfully eliminate amyloid fibrils from the brain and produce an overall significant difference in performance on cognitive assessment scales [105].”
From Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients (2024) · cites this paper as [105]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“their efficacy in improving cognitive function is limited (2, 3)”
From Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes (2024) · cites this paper as [3]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Participants who are APOE ε4 homozygous and treated with lecanemab have a 33% incidence of vasogenic oedema, ARIA-E, compared to an 11% incidence in participants who are APOE ε4 heterozygous, and 5% who are not APOE ε4 carriers. (460)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [460]
The cited source says what the claim attributes to it.
In the citing paper
“Lecanemab was associated with less worsening by 0.45 (0.23-0.67) CDR-SB points compared to placebo worsening after 18 months' treatment and in secondary cognitive, activities of daily living, and compositive outcomes. (460)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [460]
The cited source says what the claim attributes to it.
In the citing paper
“infusion-related reactions, in about 26% of patients on lecanemab, and only 7.4% of patients on placebo. (507) (460, 461)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [460]
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In the citing paper
“New drugs, including sodium oligomannate (9, GV-971),54–56 aducanumab (1),57–59 lecanemab (2),60–62 and donanemab (10, currently under review for market approval),63 which aim to offer disease-modifying therapies that intervene in the progression of AD.”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [62]
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In the citing paper
“Approximately 20% of Lecanemab trial participants and 30% of Donanemab trial participants were in stage 4 according to the CDR global score (0.5—stage 3; 1—stage 4).10,20”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“Recent clinical trials demonstrating a slowing of cognitive and functional decline in individuals with AD treated with anti-Aβ antibodies indeed reinforce the important role of Aβ in AD pathophysiology [1,2].”
From Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease (2024) · cites this paper as [1]
The cited source says what the claim attributes to it.
In the citing paper
“Focusing on lecanemab, clinical trials of the drug showed moderate slowing of cognitive and functional decline in individuals with mild cognitive impairment (MCI) or mild dementia due to Alzheimer's.”
From 2024 Alzheimer's disease facts and figures (2024) · cites this paper as [58]
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In the citing paper
“These interventions have demonstrated a modest capacity to reduce cognitive decline in select patient subgroups, but are associated with the risk of side effects, including brain swelling and microhemorrhages.”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Van Dyck et al. 2023
The cited source says what the claim attributes to it.
In the citing paper
“These interventions have demonstrated a modest capacity to reduce cognitive decline in select patient subgroups, but are associated with the risk of side effects, including brain swelling and microhemorrhages.”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Van Dyck et al. 2023
The cited source says what the claim attributes to it.
In the citing paper
“The first therapies for AD targeting the removal of amyloid are now being approved with modest positive outcomes, although associated with several side effects (Sims et al. 2023; Mintun et al. 2021; Van Dyck et al. 2023).”
From Alzheimer's Protection by PLCγ2 Compacts Plaques, Redistributes Microglia, and Protects Synapses in App NL ‐G‐F Mice (2026) · cites this paper as Van Dyck et al. 2023
The cited source says what the claim attributes to it.
In the citing paper
“Importantly, ApoE ε4 status has gained direct clinical relevance in the anti-amyloid era”
From Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era (2026) · cites this paper as [5]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The FDA approved lecanemab in July 2023. (460)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [460]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The average wait times for dementia specialists are projected to exceed 40 months by 2027”
From Review of Artificial Intelligence for Clinical Use in Alzheimer's Disease and Related Dementias (2026) · cites this paper as [12]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“with rural areas facing three times longer delays compared to urban regions.12”
From Review of Artificial Intelligence for Clinical Use in Alzheimer's Disease and Related Dementias (2026) · cites this paper as [12]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“In January 2023, Lecanemab, the other antibody for Aβ, was also approved by using the US FDA’s accelerated approval pathway as a treatment for early AD.530”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [530]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The V-PLEX platform offers analytically validated singleplex and multiplex assay kits, which can provide accurate and reproducible results with consistency from lot to lot (van Dyck et al., 2023).”
From β-amyloid accumulation enhances microtubule associated protein tau pathology in an APPNL-G-F/MAPTP301S mouse model of Alzheimer’s disease (2024) · cites this paper as van Dyck et al., 2023
Experimental — accuracy not yet measuredIn the citing paper
“In January 2023, FDA approved a new monoclonal antibody against Aβ called lecanemab for the treatment of early AD, also by its accelerated approval pathway.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [10]
In the citing paper
“Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial.”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [10]
In the citing paper
“Lecanemab reduced brain amyloid burden markedly in early AD and cognitive decline moderately than placebo at 18 months but was related to adverse events [10].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [10]
In the citing paper
“There is insufficient safety or efficacy information on starting treatment sooner or later than in the conducted studies [137,138,139].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [139]
In the citing paper
“It reported favorable outcomes for all primary and secondary measures, including ADAS-Cog14, AD Composite Score (ADCOMS), and ADCS-MCI-ADL scores [43].”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [43]
In the citing paper
“Since the positive outcomes in terms of slow decline in cognitive abilities in the lecanemab Clarity AD trial [43] and the donanemab trial TRAILBLAZER-ALZ [86], the impact of amyloid and consequent pathological alterations is likely to become the main focus of clinical trials.”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [43]
In the citing paper
“CDR-SB Score(difference: − 0.45; 95% CI: -0.67 to − 0.23)”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as Dyck et al. [2023]
In the citing paper
“Both trials (NCT03887455 and NCT01760005) had a overall low risk of bias [43, 53, 83, 84].”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [43]
In the citing paper
“Two articles reported the results of NCT03887455 [43, 84], and the other two reported the results of NCT01760005 [53, 83].”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [43]
In the citing paper
“Two anti‐amyloid monoclonal antibodies (AA‐MABS)—aducanumab and lecanemab—that slow the cognitive decline of AD are approved and another—donanemab—is currently under review.”
From Alzheimer’s disease drug development pipeline: 2024 (2024) · cites this paper as [7]
In the citing paper
“18 months of treatment with lecanemab, a humanized IgG1 monoclonal antibody targeting Aβ soluble protofibrils, reduced markers of amyloid and moderately improved cognitive decline in patients with early AD.50”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [50]
In the citing paper
“So far, two antibody-based drugs aducanumab and lecanemab have been approved by the FDA”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [50]
In the citing paper
“The results were just published and showed that patients with lecanemab treatment had lower brain amyloid levels and reduced cognitive and functional decline as measured by the Clinical Dementia Rating-Sum of Boxes (CDR-SB), which quantifies symptom severity across a range of cognitive and function domains, by 27% compared with placebo.50”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [50]
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Positive Allosteric Modulators of Trk Receptors for the Treatment of Alzheimer’s Disease
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Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain
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Nuclear SphK2/S1P signaling is a key regulator of ApoE production and Aβ uptake in astrocytes
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Enhancing early detection of cognitive impairment in primary care with the TabCAT-BHA
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PENSIEVE-AI a brief cognitive test to detect cognitive impairment across diverse literacy
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BackgroundWhat the gantenerumab trials teach us about Alzheimer's treatment
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Integrative network analysis reveals novel moderators of Aβ-Tau interaction in Alzheimer's disease
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The MR1/MAIT cell axis enhances dystrophic neurite development in Alzheimer's disease
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Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk
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Plasma ApoE proteotyping for ApoE ε4 stratification in the anti-amyloid therapies era
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Tumor-derived cystatin C enables amyloid clearance
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Reverse the progression of Alzheimer’s disease through Nano-ERASER-based adult neuroregeneration
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Is there a role for B cells in Alzheimer's disease?
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NAD+ hydrolase Sarm1 is a key driver of synapse degeneration and memory loss in Alzheimer’s disease
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Metadata
- Authors
- van Dyck, C. H., Swanson, C. J., Aisen, P., Bateman, R. J., Chen, C., Gee, M., Kanekiyo, M., Li, D., Reyderman, L., Cohen, S., Froelich, L., Katayama, S., Sabbagh, M., Vellas, B., Watson, D., Dhadda, S., Irizarry, M., Kramer, L. D., & Iwatsubo, T.
- Affiliations
- From the Alzheimer’s Disease Research Unit, Yale School of Medicine, New Haven, CT (C.H.D.); Eisai, Nutley, NJ (C.J.S., M.K., D.L., L.R., S.D., M.I., L.D.K.); the Alzheimer’s Therapeutic Research Institute, University of Southern California, San Diego (P.A.); Washington University School of Medicine in St. Louis, St. Louis (R.B.); the Memory, Aging, and Cognition Center, Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore (C.C.); Eisai, Hatfield, United Kingdom (M.G.); Toronto Memory Program, Toronto (S.C.); Medical Faculty Mannheim, University of Heidelberg, Central Institute of Mental Health, Mannheim, Germany (L.F.); Katayama Medical Clinic, Okayama (S.K.), and the Department of Neuropathology, Graduate School of Medicine, University of Tokyo, and the National Center of Neurology and Psychiatry, Tokyo (T.I.) — all in Japan; Barrow Neurological Institute, Phoenix, AZ (M.S.); Toulouse Gerontopole University Hospital, Université Paul Sabatier, INSERM Uni...
- University of Southern California (US)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2023-01-05
- Volume
- 388
- Issue
- 1
- Pages
- 9-21
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W4310461604
- Cited by
- 5,678
- References
- 27
- Citations by year
- 2026: 1501 · 2025: 1653 · 2024: 1577 · 2023: 927
- FWCI
- 652.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- HAL (submittedVersion)
- Funders
- Eisai
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- lecanemab, early Alzheimer's disease, amyloid-beta protofibrils, anti-amyloid monoclonal antibodies, amyloid PET, mild cognitive impairment, mild dementia, CDR-SB, cognitive decline, brain amyloid burden, cerebrospinal fluid biomarkers, adverse events, anti-drug antibodies, immunogenicity, Alzheimer's disease
- MeSH terms
- Activities of Daily Living, Alzheimer Disease, Cognition, Double-Blind Method, Humans, Amyloid beta-Peptides, Nootropic Agents, Antibodies, Monoclonal, Humanized
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