Donanemab in Early Symptomatic Alzheimer Disease: The TRAILBLAZER-ALZ 2 Randomized Clinical Trial
Open accessAbstract
Importance: There are limited efficacious treatments for Alzheimer disease. Objective: To assess efficacy and adverse events of donanemab, an antibody designed to clear brain amyloid plaque. Design, Setting, and Participants: Multicenter (277 medical research centers/hospitals in 8 countries), randomized, double-blind, placebo-controlled, 18-month phase 3 trial that enrolled 1736 participants with early symptomatic Alzheimer disease (mild cognitive impairment/mild dementia) with amyloid and low/medium or high tau pathology based on positron emission tomography imaging from June 2020 to November 2021 (last patient visit for primary outcome in April 2023). Interventions: Participants were randomized in a 1:1 ratio to receive donanemab (n = 860) or placebo (n = 876) intravenously every 4 weeks for 72 weeks. Participants in the donanemab group were switched to receive placebo in a blinded manner if dose completion criteria were met. Main Outcomes and Measures: The primary outcome was change in integrated Alzheimer Disease Rating Scale (iADRS) score from baseline to 76 weeks (range, 0-144; lower scores indicate greater impairment). There were 24 gated outcomes (primary, secondary, and exploratory), including the secondary outcome of change in the sum of boxes of the Clinical Dementia Rating Scale (CDR-SB) score (range, 0-18; higher scores indicate greater impairment). Statistical testing allocated α of .04 to testing low/medium tau population outcomes, with the remainder (.01) for combined population outcomes. Results: Among 1736 randomized participants (mean age, 73.0 years; 996 [57.4%] women; 1182 [68.1%] with low/medium tau pathology and 552 [31.8%] with high tau pathology), 1320 (76%) completed the trial. Of the 24 gated outcomes, 23 were statistically significant. The least-squares mean (LSM) change in iADRS score at 76 weeks was −6.02 (95% CI, −7.01 to −5.03) in the donanemab group and −9.27 (95% CI, −10.23 to −8.31) in the placebo group (difference, 3.25 [95% CI, 1.88-4.62]; P < .001) in the low/medium tau population and −10.2 (95% CI, −11.22 to −9.16) with donanemab and −13.1 (95% CI, −14.10 to −12.13) with placebo (difference, 2.92 [95% CI, 1.51-4.33]; P < .001) in the combined population. LSM change in CDR-SB score at 76 weeks was 1.20 (95% CI, 1.00-1.41) with donanemab and 1.88 (95% CI, 1.68-2.08) with placebo (difference, −0.67 [95% CI, −0.95 to −0.40]; P < .001) in the low/medium tau population and 1.72 (95% CI, 1.53-1.91) with donanemab and 2.42 (95% CI, 2.24-2.60) with placebo (difference, −0.7 [95% CI, −0.95 to −0.45]; P < .001) in the combined population. Amyloid-related imaging abnormalities of edema or effusion occurred in 205 participants (24.0%; 52 symptomatic) in the donanemab group and 18 (2.1%; 0 symptomatic during study) in the placebo group and infusion-related reactions occurred in 74 participants (8.7%) with donanemab and 4 (0.5%) with placebo. Three deaths in the donanemab group and 1 in the placebo group were considered treatment related. Conclusions and Relevance: Among participants with early symptomatic Alzheimer disease and amyloid and tau pathology, donanemab significantly slowed clinical progression at 76 weeks in those with low/medium tau and in the combined low/medium and high tau pathology population. Trial Registration: ClinicalTrials.gov Identifier: NCT04437511
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Recent 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 Sims et al. 2023
The Primary Outcome section reports that donanemab slowed decline on a cognition-and-function scale by 35.1% in the low/medium-tau group and 22.3% in the combined group versus placebo. The Discussion explicitly calls the benefit clinically meaningful, contrary to describing the benefit as minimal. This trial evaluates donanemab, not every anti-Aβ antibody. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredPhase 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 [462]
The Trial Design and Participants section says the phase 3 donanemab trial required amyloid pathology confirmed by PET for enrollment. The paper mentions a phase 2 donanemab trial and studies of aducanumab and lecanemab, but the passages do not establish their enrollment requirements or those of gantenerumab trials. No page number is available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredPost-diagnosis management challenges are increasing because new therapeutics require intensive monitoring.
“After diagnosis, challenges with management are growing as new therapeutics with intensive requirements for monitoring are emerging, adding both urgency and complexity.13,14”
From Review of Artificial Intelligence for Clinical Use in Alzheimer's Disease and Related Dementias (2026) · cites this paper as [13]
The Randomization and Intervention section describes scheduled MRIs, additional imaging every 4 to 6 weeks when abnormalities were detected, and criteria for interrupting and resuming donanemab. This supports intensive monitoring for one therapy, but the trial does not establish that post-diagnosis management challenges are increasing as new therapies emerge. Page numbers were not available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn the TRAILBLAZER-ALZ2 phase 3 study, donanemab treatment significantly slowed cognitive decline on the primary outcome of the integrated AD Rating Scale (iADRS) by 40% and improved all secondary clinical endpoints.
“On 4 May 2023, Lilly announced positive results for this phase 3 study, as treatment significantly slowed cognitive decline on the primary outcome of the integrated AD Rating Scale (iADRS) by 40% and improved all secondary clinical endpoints [68,69].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [68]
The Primary Outcome section reports significant slowing on iADRS, but the reported figures are 35.1% in the low/medium tau population and 22.3% in the combined population—not 40%. The Clinical Assessments section reports benefits on several secondary clinical measures, but the paper does not establish that all secondary clinical endpoints improved. Page numbers were not available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredChEIs are still the primary treatment for mild Alzheimer's disease, enhancing acetylcholine levels to support cognitive and functional abilities.
“ChEIs are still the primary treatment for mild AD, enhancing acetylcholine levels to support cognitive and functional abilities.9,19”
From A 2025 update on treatment strategies for the Alzheimer’s disease spectrum (2025) · cites this paper as [19]
The baseline-characteristics table (section labeled Conclusions; page unavailable) reports acetylcholinesterase inhibitor and/or memantine use among participants with early symptomatic Alzheimer disease. It does not separate ChEI use from memantine, establish ChEIs as the primary treatment for mild disease, or discuss acetylcholine levels or benefits to cognition and function. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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 Sims et al. 2023
The Discussion reports that donanemab removed amyloid plaques and slowed clinical progression, while the Adverse Events section reports imaging abnormalities and infusion reactions. The paper supports benefit and side effects for this treatment, but the passages in our copy do not establish the claim that these therapies were being approved. (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 [12]
The Clinical Assessments section reports amyloid clearance with donanemab and 28.9% slower clinical progression on the CDR-SB scale in the combined population. The paper describes promising plaque clearance with lecanemab, but does not give a 25–30% slowing figure for it or substantiate the approval years in the citing sentence. (LLM, conf=0.88)
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 [12]
The introductory passage reports promising amyloid plaque clearance for aducanumab, lecanemab, and donanemab. The Primary Outcome and Discussion report statistically significant clinical effects for donanemab, but our copy does not establish statistically significant clinical effects for the other two antibodies. The Discussion also characterizes donanemab’s benefit as clinically meaningful rather than modest. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTherapeutics relying on IgG antibodies, if administered excessively, might induce aging-related defects.
“our results raise a caution that therapeutics relying on IgG antibodies, if administered excessively, might induce aging-related defects.”
From Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging (2024) · cites this paper as [75]
The paper identifies donanemab as an IgG1 monoclonal antibody and reports treatment-associated adverse events (Introduction; Adverse Events, page unavailable). It does not show that excessive administration causes aging-related defects; the Limitations section says the 76-week follow-up limits understanding of long-term effects (page unavailable). The broader caution is the citing authors’ inference, not a finding of this trial. (LLM, conf=0.78)
Experimental — accuracy not yet measuredThe TRAILBLAZER-ALZ 2 trial suggested that donanemab provided greater benefit when initiated at an earlier disease stage indicated by less tau accumulation using tau-PET.
“Furthermore, results from the TRAILBLAZER‐ALZ 2 Randomized Clinical Trial have suggested that the amyloid‐lowering therapy donanemab provided a greater benefit when initiated at an earlier disease stage (as was indicated by less tau accumulation using tau‐PET). 46”
From Machine learning prediction of tau‐PET in Alzheimer's disease using plasma, MRI, and clinical data (2025) · cites this paper as [46]
Donanemab reported less worsening in integrated Alzheimer Disease Rating Scale (cognition and functioning) in the drug group −10.19 (−11.22 to −9.16) compared to placebo worsening −13.11 (−14.10 to −12.13) after 18 months' treatment, and in secondary cognitive, activities of daily living, and composite outcomes.
“Donanemab reported less worsening in integrated Alzheimer Disease Rating Scale (cognition and functioning) in the drug group -10.19 (-11.22 to -9.16) compared to placebo worsening -13.11 (-14.10 to -12.13) after 18 months' treatment and in secondary cognitive, activities of daily living, and composite outcomes. (462)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [462]
Diagnosing and treating people earlier in the course of AD may lead to greater clinical benefit.
“The results of TRAILBLAZER-ALZ 2 show that diagnosing and treating people earlier in the course of AD may lead to greater clinical benefit [68,69].”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [68]
Donanemab significantly slowed the clinical progression in individuals with early symptomatic AD and amyloid and tau pathology.
“Donanemab significantly slowed the clinical progression in individuals with early symptomatic AD and amyloid and tau pathology.”
From Treatment of Alzheimer’s Disease: Beyond Symptomatic Therapies (2023) · cites this paper as [68]
Accumulation 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 [2]
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 [2]
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 Sims 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 Sims et al. 2023
In TRAILBLAZER-ALZ 2, adverse effects included amyloid-related imaging problems (24% donanemab vs. 2.1% placebo).
“Adverse effects included amyloid-related imaging problems (24% donanemab vs. 2.1% placebo) and infusion-related reactions (8.7% donanemab vs. 0.5% placebo).”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [50]
In TRAILBLAZER-ALZ 2, adverse effects included infusion-related reactions (8.7% donanemab vs. 0.5% placebo).
“Adverse effects included amyloid-related imaging problems (24% donanemab vs. 2.1% placebo) and infusion-related reactions (8.7% donanemab vs. 0.5% placebo).”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [50]
Donanemab reduced decline by 60% in patients with early-stage AD.
“The drug notably reduced decline by 60% in patients with early-stage AD, supporting the efficacy of short-term dosing.”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [50]
In TRAILBLAZER-ALZ 2, donanemab achieved significant cognitive improvement in the low/medium tau group (iADRS change: −6.02 vs. −9.27 placebo).
“Donanemab achieved significant cognitive improvement in the low/medium tau group (iADRS change: − 6.02 vs. − 9.27 placebo) and combined population (change: − 10.2 vs. − 13.1 placebo).”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [50]
In TRAILBLAZER-ALZ 2, donanemab achieved significant cognitive improvement in the combined population (change: −10.2 vs. −13.1 placebo).
“Donanemab achieved significant cognitive improvement in the low/medium tau group (iADRS change: − 6.02 vs. − 9.27 placebo) and combined population (change: − 10.2 vs. − 13.1 placebo).”
From Clinical trials of new drugs for Alzheimer disease: a 2020–2023 update (2023) · cites this paper as [50]
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 [6]
Anti-amyloid monoclonal antibodies aducanumab, lecanemab, and donanemab have been approved by the US Food and Drug Administration for Alzheimer's disease.
“with the approval by the US Food and Drug Administration (FDA) of the anti-amyloid monoclonal antibodies aducanumab, lecanemab, and donanemab [11, 12].”
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- Authors
- Sims, J. R., Zimmer, J. A., Evans, C. D., Lu, M., Ardayfio, P., Sparks, J., Wessels, A. M., Shcherbinin, S., Wang, H., Monkul Nery, E. S., Collins, E. C., Solomon, P., Salloway, S., Apostolova, L. G., Hansson, O., Ritchie, C., Brooks, D. A., Mintun, M., Skovronsky, D. M., TRAILBLAZER-ALZ 2 Investigators, Abreu, R., Agarwal, P., Aggarwal, P., Agronin, M., Allen, A., Altamirano, D., Alva, G., Andersen, J., Anderson, A., Anderson, D., Arnold, J., Asada, T., Aso, Y., Atit, V., Ayala, R., Badruddoja, M., Badzio-jagiello, H., Bajacek, M., Barton, D., Bear, D., Benjamin, S., Bergeron, R., Bhatia, P., Black, S., Block, A., Bolouri, M., Bond, W., Bouthillier, J., Brangman, S., Brew, B., Brisbin, S., Brisken, T., Brodtmann, A., Brody, M., Brosch, J., Brown, C., Brownstone, P., Bukowczan, S., Burns, J., Cabrera, A., Capote, H., Carrasco, A., Cevallos Yepez, J., Chavez, E., Chertkow, H., Chyrchel-paszkiewicz, U., Ciabarra, A., Clemmons, E., Cohen, D., Cohen, R., Cohen, I., Concha, M., Costell, B., Crimmins, D., Cruz-pagan, Y., Cueli, A., Cupelo, R., Czarnecki, M., Darby, D., Dautzenberg, P. L. J., De Deyn, P., De La Gandara, J., Deck, K., Dibenedetto, D., Dibuono, M., Dinnerstein, E., Dirican, A., Dixit, S., Dobryniewski, J., Drake, R., Drysdale, P., Duara, R., Duffy, J., Ellenbogen, A., Faradji, V., Feinberg, M., Feldman, R., Fishman, S., Flitman, S., Forchetti, C., Fraga, I., Frank, A., Frishberg, B., Fujigasaki, H., Fukase, H., Fumero, I., Furihata, K., Galloway, C., Gandhi, R., George, K., Germain, M., Gitelman, D., Goetsch, N., Goldfarb, D., Goldstein, M., Goldstick, L., Gonzalez Rojas, Y., Goodman, I., Greeley, D., Griffin, C., Grigsby, E., Grosz, D., Hafner, K., Hart, D., Henein, S., Herskowitz, B., Higashi, S., Higashi, Y., Ho, G., Hodgson, J., Hohenberg, M., Hollenbeck, L., Holub, R., Hori, T., Hort, J., Ilkowski, J., Ingram, K. J., Isaac, M., Ishikawa, M., Janu, L., Johnston, M., Julio, W., Justiz, W., Kaga, T., Kakigi, T., Kalafer, M., Kamijo, M., Kaplan, J., Karathanos, M., Katayama, S., Kaul, S., Keegan, A., Kerwin, D., Khan, U., Khan, A., Kimura, N., Kirk, G., Klodowska, G., Kowa, H., Kutz, C., Kwentus, J., Lai, R., Lall, A., Lawrence, M., Lee, E., Leon, R., Linker, G., Lisewski, P., Liss, J., Liu, C., Losk, S., Lukaszyk, E., Lynch, J., Macfarlane, S., Macsweeney, J., Mannering, N., Markovic, O., Marks, D., Masdeu, J., Matsui, Y., Matsuishi, K., Mcallister, P., Mcconnehey, B., Mcelveen, A., Mcgill, L., Mecca, A., Mega, M., Mensah, J., Mickielewicz, A., Minaeian, A., Mocherla, B., Murphy, C., Murphy, P., Nagashima, H., Nair, A., Nair, M., Nardandrea, J., Nash, M., Nasreddine, Z., Nishida, Y., Norton, J., Nunez, L., Ochiai, J., Ohkubo, T., Okamura, Y., Okorie, E., Olivera, E., O'mahony, J., Omidvar, O., Ortiz-Cruz, D., Osowa, A., Papka, M., Parker, A., Patel, P., Patel, A., Patel, M., Patry, C., Peckham, E., Pfeffer, M., Pietras, A., Plopper, M., Porsteinsson, A., Poulin Robitaille, R., Prins, N., Puente, O., Ratajczak, M., Rhee, M., Ritter, A., Rodriguez, R., Rodriguez Ables, L., Rojas, J., Ross, J., Royer, P., Rubin, J., Russell, D., Rutgers, S. M., Rutrick, S., Sadowski, M., Safirstein, B., Sagisaka, T., Scharre, D., Schneider, L., Schreiber, C., Schrift, M., Schulz, P., Schwartz, H., Schwartzbard, J., Scott, J., Selem, L., Sethi, P., Sha, S., Sharlin, K., Sharma, S., Shiovitz, T., Shiwach, R., Sladek, M., Sloan, B., Smith, A., Solomon, P., Sorial, E., Sosa, E., Stedman, M., Steen, S., Stein, L., Stolyar, A., Stoukides, J., Sudoh, S., Sutton, J., Syed, J., Szigeti, K., Tachibana, H., Takahashi, Y., Tateno, A., Taylor, J. D., Taylor, K., Tcheremissine, O., Thebaud, A., Thein, S., Thurman, L., Toenjes, S., Toji, H., Toma, M., Tran, D., Trueba, P., Tsujimoto, M., Turner, R., Uchiyama, A., Ussorowska, D., Vaishnavi, S., Valor, E., Vandersluis, J., Vasquez, A., Velez, J., Verghese, C., Vodickova-borzova, K., Watson, D., Weidman, D., Weisman, D., White, A., Willingham, K., Winkel, I., Winner, P., Winston, J., Wolff, A., Yagi, H., Yamamoto, H., Yathiraj, S., Yoshiyama, Y., & Zboch, M.
- Affiliations
- Eli Lilly (United States) (US)
- Eli Lilly and Company, Indianapolis, Indiana
- Brown University (US)
- Indiana University School of Medicine (US)
- Lund University (SE)
- Scottish Brain Sciences, Edinburgh, United Kingdom
- for the TRAILBLAZER-ALZ 2 Investigators
- Corresponding author
- Sims, John R.
- ORCID
- Sims, John R.
- Lu, Ming
- Ardayfio, Paul
- Wessels, Alette M.
- Shcherbinin, Sergey
- Wang, Hong
- Collins, Emily C.
- Salloway, Stephen
- Apostolova, Liana G.
- Hansson, Oskar
- Ritchie, Craig
- Brooks, Dawn A.
- Agarwal, Pinky
- Aggarwal, Puja
- Agronin, Marc
- Alva, Gustavo
- Anderson, Donald
- Asada, Takashi
- Aso, Yasuhiro
- Bergeron, Richard
- Bhatia, Perminder
- Black, Sandra
- Brangman, Sharon
- Brodtmann, Amy
- Brosch, Jared
- Burns, Jeffrey
- Chertkow, Howard
- Chyrchel-paszkiewicz, Urszula
- Concha, Mauricio
- Darby, David
- Dautzenberg, P.l.j.
- Dibenedetto, David
- Duara, Ranjan
- Ellenbogen, Aaron
- Frank, Andrew
- Fukase, Hiroyuki
- Gitelman, Darren
- Goodman, Ira
- Greeley, David
- Hart, David
- Higashi, Shinji
- Ho, Gilbert
- Hodgson, Jonathan
- Hohenberg, Mark
- Hori, Tomokatsu
- Hort, Jakub
- Ilkowski, Jan
- Johnston, Mark
- Kerwin, Diana
- Kimura, Noriyuki
- Kirk, Gregory
- Kowa, Hisatomo
- Liss, Jonathan
- Macfarlane, Stephen
- Macsweeney, Josephine
- Masdeu, Joseph
- Matsuishi, Kunitaka
- Mcallister, Peter
- Mecca, Adam
- Mega, Michael
- Murphy, Paul
- Nair, Anil
- Ohkubo, Takuya
- Omidvar, Omid
- Patel, Ashok
- Patel, Meenakshi
- Porsteinsson, Anton
- Prins, Niels
- Rodriguez, Ramon
- Rojas, Julio
- Ross, Jeffrey
- Russell, David
- Rutrick, Stephanie
- Sadowski, Martin
- Scharre, Douglas
- Schneider, Lon
- Schrift, Michael
- Schulz, Paul
- Schwartz, Harvey
- Sha, Sharon
- Sharma, Sanjiv
- Sorial, Ehab
- Szigeti, Kinga
- Takahashi, Yuichi
- Tateno, Amane
- Tsujimoto, Masashi
- Turner, Raymond
- Vaishnavi, Sanjeev
- Verghese, Cherian
- Watson, David
- Yoshiyama, Yasumasa
- Zboch, Marzena
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2023-08-08
- Volume
- 330
- Issue
- 6
- Pages
- 512
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC10352931
- OpenAlex
- W4384522480
- Cited by
- 2,932
- References
- 40
- Citations by year
- 2026: 1022 · 2025: 1006 · 2024: 749 · 2023: 155
- FWCI
- 523.53
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Funders
- Eli Lilly and Company
- National Institutes of Health (1s10od025214-01)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- donanemab, Alzheimer's disease, amyloid plaque clearance, anti-amyloid antibodies, mild cognitive impairment, mild dementia, tau pathology, Clinical Dementia Rating, cognitive decline, treatment efficacy, adverse events, PET imaging biomarkers, trial discontinuation, intravenous infusion safety
- MeSH terms
- Aged, Alzheimer Disease, Antibodies, Monoclonal, Brain, Double-Blind Method, Female, Humans, Male, Treatment Outcome, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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