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 aducanumab, lecanemab, donanemab, and gantenerumab targeting Aβ required PET or CSF evidence of amyloid pathology for trial enrolment.
“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]
The Eligibility Criteria section (page not provided) says that amyloid positivity for the phase 3 lecanemab trial was determined by PET or CSF testing. The paper mentions a phase 2b lecanemab trial and cites studies of aducanumab and donanemab, but it does not establish the stated enrolment requirement for those trials or for gantenerumab trials. (LLM, conf=0.88)
Experimental — accuracy not yet measuredAdding anti-amyloid therapy to ChEI treatment in early-stage Alzheimer's disease can maintain cognitive function better and longer (5-10 years).
“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]
The Trial Design and Oversight section says participants could be taking acetylcholinesterase inhibitors, and Table 2 reports less cognitive decline with lecanemab than placebo at 18 months. The paper does not establish a benefit specifically from adding lecanemab to ChEI treatment or show that cognitive function is maintained for 5–10 years; the Discussion says longer trials are needed. (LLM, conf=0.90)
Experimental — accuracy not yet measuredAnti-amyloid immunotherapy including the FDA-approved monoclonal antibodies lecanemab and donanemab has proven efficacy in slowing cognitive decline in early-stage Alzheimer's disease.
“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]
The Abstract reports moderately less decline in cognition and function with lecanemab than with placebo over 18 months in people with early Alzheimer’s disease. The paper does not report efficacy for donanemab; its introductory section (10) identifies aducanumab, not lecanemab or donanemab, as having received FDA approval. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThe FDA approved lecanemab and donanemab for "early-stage" Alzheimer's disease, encompassing both stage 3 (MCI) and stage 4 (mild dementia).
“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]
The Abstract and Eligibility Criteria define early Alzheimer’s disease in the lecanemab trial as mild cognitive impairment or mild dementia. The paper does not state that the FDA approved lecanemab or donanemab, or identify these conditions as stages 3 and 4; its introduction mentions accelerated FDA approval of aducanumab instead. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAnti-amyloid immunotherapy with lecanemab or donanemab is now considered as an add-on therapy for mild Alzheimer's disease.
“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]
The Trial Design and Oversight section studied lecanemab in people with early Alzheimer’s disease and allowed concomitant approved symptomatic medications, supporting its potential use alongside existing treatment. The paper does not establish that lecanemab is now considered an add-on therapy in clinical practice, and it does not establish that claim for donanemab. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Lecanemab received traditional approval from the FDA for treatment of patients with MCI and mild dementia with biomarker-proven Aβ pathology.
“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]
The Abstract describes a lecanemab trial in patients with mild cognitive impairment or mild dementia due to Alzheimer’s disease and biomarker evidence of amyloid. The introduction (section 10) mentions FDA approval only for aducanumab; our copy does not substantiate the claim that lecanemab received traditional FDA approval. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAnti-amyloid antibodies can clear Aβ plaques from the brain, leading to a slowing of cognitive and functional decline in individuals with MCI and mild dementia due to AD.
“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]
The Abstract reports that, in a phase 3 trial of people with MCI or mild dementia due to Alzheimer’s disease, lecanemab reduced brain amyloid burden and produced moderately less cognitive and functional decline than placebo at 18 months. The paper does not establish that plaque removal itself caused the slower decline; its introduction says only that some evidence suggests amyloid removal slows disease progression. (LLM, conf=0.83)
Experimental — accuracy not yet measuredIn patients with early-stage AD, coexistence of pathology from other etiologies, such as VD, can increase the risk of amyloid-related imaging abnormalities.
“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]
The Eligibility Criteria describe participants with early Alzheimer’s disease, and the Safety and Discussion sections report amyloid-related imaging abnormalities (ARIA) during lecanemab treatment. The paper does not report that coexisting pathology from another etiology, such as vascular dementia, increases ARIA risk; its reported variation in ARIA frequency concerns ApoE ε4 status. (LLM, conf=0.81)
Experimental — accuracy not yet measuredAccumulation of amyloid beta is an early critical hallmark of Alzheimer's disease and an important target for understanding pathophysiology and therapy.
“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]
The Abstract says aggregated Aβ may initiate or potentiate pathological processes in Alzheimer’s disease, and the paper tests an Aβ-targeting therapy in people with early disease. It does not establish that Aβ accumulation is an early, critical hallmark; the claim states that significance more definitively than the source does. (LLM, conf=0.84)
Experimental — accuracy not yet measuredCurrent FDA-approved treatments offer modest symptomatic benefit or partial slowing of progression but do not halt neurodegeneration or restore lost neuronal circuits.
“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]
The introduction (p. 10) says existing therapeutic agents temporarily improve symptoms without altering the underlying disease course, and that amyloid removal may slow progression. The Discussion reports moderately less clinical decline with lecanemab over 18 months. The paper does not establish the broader claims that FDA-approved treatments cannot halt neurodegeneration or restore lost neuronal circuits. (LLM, conf=0.84)
Experimental — accuracy not yet measuredRecent therapies targeting Aβ clearance using anti-Aβ monoclonal antibodies during early stages of AD provide minimal cognitive benefit.
“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
The Abstract and Discussion report that lecanemab reduced brain amyloid and produced moderately less decline in cognition and function than placebo at 18 months in people with early Alzheimer’s disease. The paper does not characterize that benefit as “minimal,” and its trial of one antibody does not establish the claim about therapies in general. (LLM, conf=0.85)
Experimental — accuracy not yet measuredLecanemab and donanemab clear Aβ plaque deposits and slow cognitive decline by 25 to 30%.
“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]
The End-Point Results report that lecanemab reduced brain amyloid burden and that CDR-SB worsening at 18 months was 1.21 versus 1.66 with placebo—approximately 27% less decline on that measure. The paper does not establish the claimed effects for donanemab or substantiate the stated approval dates. (LLM, conf=0.91)
Experimental — accuracy not yet measuredAnti-amyloid monoclonal antibodies aducanumab, lecanemab, and donanemab have demonstrated robust amyloid clearance with statistically significant but modest clinical effects.
“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]
The Results (Abstract; page not provided) report a large reduction in brain amyloid burden with lecanemab and statistically significant, modest differences in clinical outcomes versus placebo at 18 months. The paper does not report corresponding amyloid-clearance and clinical-effect results for aducanumab or donanemab, so it supports the claim only for lecanemab. (LLM, conf=0.90)
Experimental — accuracy not yet measuredFDA-approved anti-Aβ monoclonal antibodies are very effective at removing Aβ from the brain parenchyma, but 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).
“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]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredε4 carriers, particularly ε4 homozygotes, exhibit a substantially increased risk of amyloid-related imaging abnormalities (ARIA) during treatment with anti-amyloid monoclonal antibodies.
“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]
The Safety section and Table 3 show higher ARIA rates among ApoE ε4 carriers receiving lecanemab, especially homozygotes: ARIA-E occurred in 5.4% of noncarriers, 15.8% of carriers, and 32.6% of homozygotes. The paper studied lecanemab specifically, so it does not by itself establish the risk across anti-amyloid monoclonal antibodies as a class. (LLM, conf=0.86)
Experimental — accuracy not yet measuredApoE genotyping is now increasingly considered an important component of the pre-treatment work-up for anti-amyloid therapies.
“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]
The Safety section reports that amyloid-related imaging abnormalities during the lecanemab trial were more frequent in ApoE ε4 carriers, especially homozygotes. That supports the relevance of genotype to treatment-risk assessment, but the paper does not say that ApoE genotyping is increasingly considered part of a pre-treatment work-up for anti-amyloid therapies generally. (LLM, conf=0.82)
Experimental — accuracy not yet measuredCurrent "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.
“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]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe efficacy of Aβ antibodies in improving cognitive function is limited.
“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]
The Abstract reports that lecanemab produced moderately less decline on measures of cognition and function than placebo over 18 months. That supports a limited cognitive benefit, but the paper studied lecanemab specifically, not Aβ antibodies as a class, and it reports slower decline rather than improved cognitive function. (LLM, conf=0.84)
Experimental — accuracy not yet measuredParticipants who are APOE ε4 homozygous and treated with lecanemab have a 33% incidence of vasogenic oedema (ARIA-E), compared to 11% in APOE ε4 heterozygous and 5% in non-carriers.
“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]
Lecanemab was associated with less worsening by 0.45 (0.23-0.67) CDR-SB points compared to placebo after 18 months' treatment, and in secondary cognitive, activities of daily living, and composite outcomes.
“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]
Infusion-related reactions occur in about 26% of patients on lecanemab and 7.4% of patients on placebo.
“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]
New drugs including sodium oligomannate, aducanumab, lecanemab, and donanemab aim to offer disease-modifying therapies that intervene in AD progression.
“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]
Approximately 20% of lecanemab trial participants and 30% of donanemab trial participants were in stage 4 according to the CDR global score.
“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]
Recent clinical trials demonstrate slowing of cognitive and functional decline in individuals with Alzheimer's disease treated with anti-amyloid beta antibodies.
“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]
Clinical trials of lecanemab showed moderate slowing of cognitive and functional decline in individuals with MCI or mild dementia due to Alzheimer's.
“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]
Monoclonal antibody interventions promoting amyloid removal are associated with risk of side effects, including brain swelling and microhemorrhages.
“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 <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Van Dyck et al. 2023
Monoclonal antibodies promoting removal of amyloid have demonstrated a modest capacity to reduce cognitive decline in select patient subgroups.
“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 <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Van Dyck et al. 2023
The first therapies for AD targeting the removal of amyloid are now being approved with modest positive outcomes, although associated with several side effects.
“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 <scp>PLCγ2</scp> Compacts Plaques, Redistributes Microglia, and Protects Synapses in <scp> <i>App</i> <sup> <i>NL</i> </sup> </scp> <sup> <i>‐G‐F</i> </sup> Mice (2026) · cites this paper as Van Dyck et al. 2023
ApoE ε4 status has gained direct clinical relevance in the anti-amyloid era.
“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 FDA approved lecanemab in July 2023.
“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]
The introduction (§10) mentions FDA accelerated approval of aducanumab, not lecanemab. Searches of our copy for lecanemab’s FDA approval and July 2023 found no passage addressing the claimed approval or date. (LLM, conf=0.75)
Experimental — accuracy not yet measuredAverage wait times for dementia specialists are projected to exceed 40 months by 2027.
“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]
The Eligibility Criteria and Discussion describe a lecanemab trial, not access to dementia specialists. Searches for specialist wait times, 40 months, and 2027 found no projection in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredRural areas face delays for dementia specialists that are three times longer than urban areas.
“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]
The Eligibility Criteria and Discussion describe a lecanemab trial, not access to dementia specialists. Searches for rural–urban differences and specialist waiting times found no passage in our copy reporting threefold longer delays in rural areas. (LLM, conf=0.75)
Experimental — accuracy not yet measuredLecanemab was approved by the US FDA's accelerated approval pathway as a treatment for early AD in January 2023.
“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]
The introduction (section 10) says that aducanumab received FDA accelerated approval, but does not say that lecanemab did. Our copy describes a trial of lecanemab in early Alzheimer’s disease; it does not establish whether or when lecanemab was approved. The approval statement about aducanumab does not rule out a later approval of lecanemab in January 2023. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThe V-PLEX platform offers analytically validated singleplex and multiplex assay kits, which can provide accurate and reproducible results with consistency from lot to lot.
“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
The Trial Design and Oversight and End Points sections describe blood testing and the biomarkers assessed, but do not identify the V-PLEX platform or discuss its assay kits. Searches for V-PLEX, singleplex and multiplex kits, assay validation, reproducibility, and lot-to-lot consistency found no supporting passage in our copy. (LLM, conf=0.75)
Experimental — accuracy not yet measuredLecanemab was approved by the FDA in January 2023 for early AD via accelerated approval.
“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]
Two anti-Aβ drugs have received accelerated FDA approval for AD treatment, but their efficacy or long-term safety is controversial.
“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]
Lecanemab reduced brain amyloid burden markedly and cognitive decline moderately compared with placebo at 18 months in early AD, but was related to adverse events.
“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]
There is insufficient safety or efficacy information on starting lecanemab treatment sooner or later than in the conducted studies.
“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]
Clarity AD reported favorable outcomes for all primary and secondary measures, including ADAS-Cog14, ADCOMS, and ADCS-MCI-ADL scores.
“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]
The impact of amyloid and consequent pathological alterations is likely to become the main focus of clinical trials.
“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 lecanemab Clarity AD trial, lecanemab reduced CDR-SB score compared to placebo (difference: −0.45; 95% CI: -0.67 to −0.23).
“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]
Both trials NCT03887455 and NCT01760005 had an overall low risk of bias.
“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]
Two articles reported the results of NCT03887455, and the other two reported the results of NCT01760005.
“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]
Two anti-amyloid monoclonal antibodies (aducanumab and lecanemab) that slow the cognitive decline of AD are approved, and donanemab is under review.
“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]
CLARITY AD showed that 18 months of lecanemab treatment reduced markers of amyloid and moderately improved cognitive decline in patients with early AD.
“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]
Two antibody-based drugs, aducanumab and lecanemab, have been approved by the FDA.
“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]
Results showed that patients with lecanemab treatment had lower brain amyloid levels and reduced cognitive and functional decline as measured by CDR-SB by 27% compared with placebo.
“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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Immunotherapies for Alzheimer’s disease
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Lecanemab: Looking Before We Leap
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Once upon a time, the Amyloid Cascade Hypothesis
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Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
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“There is insufficient safety or efficacy information on starting treatment sooner or later than in the conducted studies [137–139].”
BackgroundDiagnosis and Management of Posterior Cortical Atrophy
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Artificial intelligence for dementia drug discovery and trials optimization
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Reelin links Apolipoprotein E4, Tau, and Amyloid‐β in Alzheimer’s disease
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Microglial phagocytosis in Alzheimer disease
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Plasma ATN(I) classification and precision pharmacology in Alzheimer's disease
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Evaluation of clinical benefits of treatments for Alzheimer's disease
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A blood biomarker test for brain amyloid impacts the clinical evaluation of cognitive impairment
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A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation
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Current therapeutics for Alzheimer’s disease and clinical trials
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“In the Clarity AD trial, lecanemab was shown to slow the progression of cognitive and functional decline in patients with early-stage AD, with improvements in CSF and plasma biomarkers, including A β and phosphorylated tau, leading to subsequent full FDA approval [10].”
BackgroundInfluential
- 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 · 2022: 17 · 2021: 1 · 2012: 2
- 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
- Health Sciences › Medicine › Physiology › 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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