A Primer on the Evolution of Aducanumab: The First Antibody Approved for Treatment of Alzheimer’s Disease
Abstract
Alzheimer's disease (AD) is the most common form of dementia with global burden projected to triple by 2050. It incurs significant biopsychosocial burden worldwide with limited treatment options. Aducanumab is the first monoclonal antibody recently approved by the US-FDA for mild AD through the accelerated approval pathway. It is the first molecule to be approved for AD since 2003 and carries with it a therapeutic promise for the future. As the definition of AD has evolved from a pathological entity to a Clinico-biological construct over the years, the amyloid-β (Aβ) pathway has been increasingly implicated in its pathogenesis. The approval of Aducanumab is based on reduction of the Aβ load in the brain, which forms a surrogate marker for this pathway. The research populace has, however, been globally divided by skepticism and hope regarding this approval. Failure to meet clinical endpoints in the trials, alleged transparency issues, cost-effectiveness, potential adverse effects, need for regular monitoring, and critique of 'amyloid cascade hypothesis' itself are the main caveats concerning the antibody. With this controversy in background, this paper critically looks at antibody research in AD therapeutics, evidence, and evolution of Aducanumab as a drug and the potential clinical implications of its use in future. While the efficacy of this monoclonal antibody in AD stands as a test of time, based on the growing evidence it is vital to rethink and explore alternate pathways of pathogenesis (oxidative stress, neuroinflammation, cholesterol metabolism, vascular factors, etc.) as possible therapeutic targets that may help elucidate the enigma of this complex yet progressive and debilitating neurodegenerative disorder.
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From 2003 to 2022, only one new drug, aducanumab, was controversially approved for use in AD.
“From 2003 to 2022, only one new drug, aducanumab, was controversially approved for use in AD (Mukhopadhyay and Banerjee, 2021).”
From Drug repurposing for Alzheimer’s disease from 2012–2022—a 10-year literature review (2023) · cites this paper as Mukhopadhyay and Banerjee, 2021
Aducanumab demonstrated inconsistent outcomes in its two main Phase III clinical trials, EMERGE and ENGAGE.
“Aducanumab demonstrated inconsistent outcomes in its two main clinical trials, the Phase III EMERGE and ENGAGE research investigations.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
In the EMERGE trial, participants with AD at risk for cognitive deterioration showed a decrease in amyloid-beta plaques.
“In the EMERGE experiment, when participants with AD were at risk for cognitive deterioration, there was a decrease in the amount of amyloid-beta plaques.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
After 79 weeks, lecanemab produced a lower total brain amyloid plaque burden than placebo in Study 201.
“After 79 weeks, lecanemab was found to have a lower total brain amyloid plaque burden than a placebo (Study 201).”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
The mean difference in brain amyloid between lecanemab and placebo was −73.5 centiloides and −0.31 SUVR units.
“In particular, a mean difference of −73.5 centiloides and −0.31 standardized uptake value ratio (SUVR) units was found between the lecanemab and placebo treatment groups.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
The FDA granted expedited approval of aducanumab on the grounds of the EMERGE trial's documented decrease in amyloid levels.
“In spite of this, the FDA granted expedited approval on the grounds of the EMERGE trial’s documented decrease in amyloid levels [132,185,186,187].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
Lecanemab's capacity to lower brain amyloid, as shown by PET scans, led to its submission for expedited approval for AD treatment.
“Lecanemab’s capacity to lower the amount of amyloid in the brain, as shown by PET scans, has led to its submission for expedited approval for the treatment of AD.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
The treatment effect of lecanemab increased in a dose- and exposure-dependent manner, with 25% AUC therapy probably superior to placebo by >0.64.
“Additionally, the treatment impact increased in a dose- and exposure-dependent manner; a 25% AUC therapy was probably superior to a placebo by >0.64.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
At week 79, the study suggested a 20% to 40% risk reduction be applied to the advancement of clinical symptoms.
“The study also suggested at week 79 that a risk reduction of 20% to 40% be applied to the advancement of clinical symptoms [187,188].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [187]
Cites
1 retracted
RETRACTED: Cognitive effects of cell-derived and synthetically derived Aβ oligomers
Reed, M. N., Hofmeister, J. J., Jungbauer, L. M., Welzel, A. T., Yu, C., Sherman, M. A., Lesné, S., LaDu, M. J., Walsh, D. M., Ashe, K. H., et al. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.11.007 · Cited by 132 · see citing works
RetractedNeuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · see citing works
NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537 · see citing works
Corder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429 · see citing works
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484 · see citing works
The amyloid hypothesis of Alzheimer's disease at 25 years
Selkoe, D. J., & Hardy, J. (2016) · EMBO Molecular Medicine · doi:10.15252/emmm.201606210 · Cited by 6,164 · see citing works
Scheltens, P., De Strooper, B., Kivipelto, M., Holstege, H., Chételat, G., Teunissen, C. E., Cummings, J., & van der Flier, W. M. (2021) · The Lancet · doi:10.1016/s0140-6736(20)32205-4 · Cited by 5,465 · see citing works
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., Chi, H., Lin, C., Li, G., Holman, K., et al. (1995) · Nature · doi:10.1038/375754a0 · Cited by 4,051 · see citing works
Cognitive reserve in ageing and Alzheimer's disease
Stern, Y. (2012) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70191-6 · Cited by 3,557 · see citing works
The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease
Sevigny, J., Chiao, P., Bussière, T., Weinreb, P. H., Williams, L., Maier, M., Dunstan, R., Salloway, S., Chen, T., Ling, Y., et al. (2016) · Nature · doi:10.1038/nature19323 · Cited by 3,059 · see citing works
Nichols, E., Szoeke, C. E. I., Vollset, S. E., Abbasi, N., Abd-Allah, F., Abdela, J., Aichour, M. T. E., Akinyemi, R. O., Alahdab, F., Asgedom, S. W., et al. (2019) · The Lancet Neurology · doi:10.1016/s1474-4422(18)30403-4 · Cited by 2,412 · see citing works
2020 Alzheimer's disease facts and figures
(2020) · Alzheimer's & Dementia · doi:10.1002/alz.12068 · Cited by 2,353 · see citing works
Karran, E., Mercken, M., & Strooper, B. D. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3505 · Cited by 2,188 · cited 2× · see citing works
“…the amyloid cascade hypothesis incorporates several key pathogenic points in the process of AD and provides a practical explanation for the phenotypes, it falls short of accounting for the A (cid:2) interaction with tau, which is a central factor for the downstream neuronal damage in AD [17].”
Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease
Salloway, S., Sperling, R., Fox, N. C., Blennow, K., Klunk, W., Raskind, M., Sabbagh, M., Honig, L. S., Porsteinsson, A. P., Ferris, S., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1304839 · Cited by 1,960 · see citing works
Oxidative Damage Is the Earliest Event in Alzheimer Disease
Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., et al. (2001) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/60.8.759 · Cited by 1,885 · see citing works
Alzheimer’s disease drug-development pipeline: Few candidates, frequent failures
Cummings, J. L., Morstorf, T., & Zhong, K. (2014) · Alzheimer's Research & Therapy · doi:10.1186/alzrt269 · Cited by 1,744 · see citing works
Donanemab in Early Alzheimer’s Disease
Mintun, M. A., Lo, A. C., Duggan Evans, C., Wessels, A. M., Ardayfio, P. A., Andersen, S. W., Shcherbinin, S., Sparks, J., Sims, J. R., Brys, M., et al. (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2100708 · Cited by 1,728 · see citing works
Alzheimer’s Disease: The Challenge of the Second Century
Holtzman, D. M., Morris, J. C., & Goate, A. M. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002369 · Cited by 1,424 · see citing works
Neurotoxicity of Amyloid -Protein: Synaptic and Network Dysfunction
Mucke, L., & Selkoe, D. J. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006338 · Cited by 1,000 · see citing works
Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease
Kametani, F., & Hasegawa, M. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00025 · Cited by 836 · see citing works
Reiman, E. M., Chen, K., Liu, X., Bandy, D., Yu, M., Lee, W., Ayutyanont, N., Keppler, J., Reeder, S. A., Langbaum, J. B. S., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0900345106 · Cited by 785 · see citing works
Early Aβ accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain
Ingelsson, M., Fukumoto, H., Newell, K. L., Growdon, J. H., Hedley–Whyte, E. T., Frosch, M. P., Albert, M. S., Hyman, B. T., & Irizarry, M. C. (2004) · Neurology · doi:10.1212/01.wnl.0000115115.98960.37 · Cited by 666 · see citing works
Neuropathology of nondemented aging: presumptive evidence for preclinical Alzheimer disease
Price, J. L., McKeel, D. W., Buckles, V. D., Roe, C. M., Xiong, C., Grundman, M., Hansen, L. A., Petersen, R. C., Parisi, J. E., Dickson, D. W., et al. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2009.04.002 · Cited by 661 · see citing works
Two-year follow-up of amyloid deposition in patients with Alzheimer's disease
Engler, H., Forsberg, A., Almkvist, O., Blomquist, G., Larsson, E., Savitcheva, I., Wall, A. E., Ringheim, A., Långström, B., & Nordberg, A. K. (2006) · Brain · doi:10.1093/brain/awl178 · Cited by 614 · see citing works
Amyloid cascade hypothesis: Pathogenesis and therapeutic strategies in Alzheimer's disease
Barage, S. H., & Sonawane, K. D. (2015) · Neuropeptides · doi:10.1016/j.npep.2015.06.008 · Cited by 579 · see citing works
Anti-Amyloid-β Monoclonal Antibodies for Alzheimer’s Disease: Pitfalls and Promise
van Dyck, C. H. (2018) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.08.010 · Cited by 568 · see citing works
Alzheimer’s disease drug development pipeline: 2020
Cummings, J., Lee, G., Ritter, A., Sabbagh, M., & Zhong, K. (2020) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1002/trc2.12050 · Cited by 557 · see citing works
Knopman, D. S., Jones, D. T., & Greicius, M. D. (2021) · Alzheimer's & Dementia · doi:10.1002/alz.12213 · Cited by 524 · cited 2× · see citing works
“Knopman et al. suggested that the apparent benefit in the post-hoc subgroup was not due to the drug dose [71].”
Inconsistencies and Controversies Surrounding the Amyloid Hypothesis of Alzheimer's Disease
Morris, G. P., Clark, I. A., & Vissel, B. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0135-5 · Cited by 522 · see citing works
Alzheimer disease therapy—moving from amyloid-β to tau
Giacobini, E., & Gold, G. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2013.223 · Cited by 483 · see citing works
β-Amyloid Monomers Are Neuroprotective
Giuffrida, M. L., Caraci, F., Pignataro, B., Cataldo, S., De Bona, P., Bruno, V., Molinaro, G., Pappalardo, G., Messina, A., Palmigiano, A., et al. (2009) · The Journal of Neuroscience · doi:10.1523/jneurosci.1736-09.2009 · Cited by 421 · see citing works
Glial contributions to neurodegeneration in tauopathies
Leyns, C. E. G., & Holtzman, D. M. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0192-x · Cited by 409 · see citing works
Cognition, reserve, and amyloid deposition in normal aging
Rentz, D. M., Locascio, J. J., Becker, J. A., Moran, E. K., Eng, E., Buckner, R. L., Sperling, R. A., & Johnson, K. A. (2009) · Annals of Neurology · doi:10.1002/ana.21904 · Cited by 395 · see citing works
Anti-Aβ Therapeutics in Alzheimer's Disease: The Need for a Paradigm Shift
Golde, T. E., Schneider, L. S., & Koo, E. H. (2011) · Neuron · doi:10.1016/j.neuron.2011.01.002 · Cited by 382 · see citing works
The Amyloid Cascade Hypothesis in Alzheimer’s Disease: It’s Time to Change Our Mind
Ricciarelli, R., & Fedele, E. (2017) · Current Neuropharmacology · doi:10.2174/1570159x15666170116143743 · Cited by 380 · see citing works
Structural and kinetic basis for the selectivity of aducanumab for aggregated forms of amyloid-β
Arndt, J. W., Qian, F., Smith, B. A., Quan, C., Kilambi, K. P., Bush, M. W., Walz, T., Pepinsky, R. B., Bussière, T., Hamann, S., et al. (2018) · Scientific Reports · doi:10.1038/s41598-018-24501-0 · Cited by 364 · see citing works
The amyloid hypothesis on trial
Makin, S. (2018) · Nature · doi:10.1038/d41586-018-05719-4 · Cited by 360 · see citing works
Aβ40 Inhibits Amyloid Deposition<i>In Vivo</i>
Kim, J., Onstead, L., Randle, S., Price, R., Smithson, L., Zwizinski, C., Dickson, D. W., Golde, T., & McGowan, E. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.4849-06.2007 · Cited by 359 · cited 1× · see citing works
“Further, in A (cid:2) -overexpressing BRI2-A (cid:2) mice, A (cid:2) oligomers and plaques were observed but in the absence of neuronal loss or cognitive decline [77, 78].”
A trial of gantenerumab or solanezumab in dominantly inherited Alzheimer’s disease
Salloway, S., Farlow, M., McDade, E., Clifford, D. B., Wang, G., Llibre-Guerra, J. J., Hitchcock, J. M., Mills, S. L., Santacruz, A. M., Aschenbrenner, A. J., et al. (2021) · Nature Medicine · doi:10.1038/s41591-021-01369-8 · Cited by 359 · see citing works
Tolar, M., Abushakra, S., Hey, J. A., Porsteinsson, A., & Sabbagh, M. (2020) · Alzheimer's Research & Therapy · doi:10.1186/s13195-020-00663-w · Cited by 354 · cited 2× · see citing works
“Compared to another monoclonal antibody Gantenerumab which only showed marked biomarker effects, Aducanumab revealed better outcomes both in terms of clinical measures and biomarkers [42].”
Lipids revert inert Aβ amyloid fibrils to neurotoxic protofibrils that affect learning in mice
Martins, I. C., Kuperstein, I., Wilkinson, H. R., Maes, E., Vanbrabant, M., Jonckheere, W., Gelder, P. V., Hartmann, D., D’Hooge, R., Strooper, B. D., et al. (2007) · The EMBO Journal · doi:10.1038/sj.emboj.7601953 · Cited by 311 · see citing works
Dickson, T. C., & Vickers, J. C. (2001) · Neuroscience · doi:10.1016/s0306-4522(01)00169-5 · Cited by 294 · see citing works
Atwood, C., Obrenovich, M. E., Liu, T., Chan, H., Perry, G. L., Smith, M. A., & Martins, R. N. (2003) · Brain Research Reviews · doi:10.1016/s0165-0173(03)00174-7 · Cited by 292 · see citing works
Lee, E. B., Leng, L. Z., Zhang, B., Kwong, L. K., Trojanowski, J. Q., Abel, T. G., & Lee, V. M. ‐. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m511018200 · Cited by 252 · see citing works
Alexander, G. C., Emerson, S., & Kesselheim, A. S. (2021) · JAMA · doi:10.1001/jama.2021.3854 · Cited by 240 · see citing works
Aducanumab produced a clinically meaningful benefit in association with amyloid lowering
Cummings, J., Aisen, P., Lemere, C., Atri, A., Sabbagh, M., & Salloway, S. (2021) · Alzheimer's Research & Therapy · doi:10.1186/s13195-021-00838-z · Cited by 224 · see citing works
Copernicus revisited: amyloid beta in Alzheimer's disease.
Josepha, J. A., Shukitt-Hale, B., Denisova, N., Martín, A., Perry, G., & Smith, M. A. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00211-6 · Cited by 209 · see citing works
Ferrero, J., Williams, L., Stella, H., Leitermann, K., Mikulskis, A., O'Gorman, J., & Sevigny, J. (2016) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2016.06.002 · Cited by 189 · see citing works
Understanding the Amyloid Hypothesis in Alzheimer’s Disease
Paroni, G., Bisceglia, P., & Seripa, D. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180802 · Cited by 186 · see citing works
Castellani, R. J., Lee, H., Siedlak, S. L., Nunomura, A., Hayashi, T., Nakamura, M., Zhu, X., Perry, G. L., & Smith, M. A. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1151 · Cited by 140 · see citing works
Landmark Alzheimer’s drug approval confounds research community
Mullard, A. (2021) · Nature · doi:10.1038/d41586-021-01546-2 · Cited by 140 · see citing works
Current Alzheimer's disease clinical trials: Methods and placebo outcomes
Schneider, L. S. S., & Sano, M. C. (2009) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2009.07.038 · Cited by 137 · see citing works
The Role and Therapeutic Targeting of α-, β- and γ-Secretase in Alzheimer's Disease
MacLeod, R., Hillert, E., Cameron, R. T., & Baillie, G. S. (2015) · Future Science OA · doi:10.4155/fso.15.9 · Cited by 131 · see citing works
BETASCAN: Probable β-amyloids Identified by Pairwise Probabilistic Analysis
Bryan, A. W., Menke, M. E., Cowen, L., Lindquist, S. L., & Berger, B. (2009) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1000333 · Cited by 118 · see citing works
Behavioral symptoms and caregiver burden in dementia
Shaji, K., George, R. K., Prince, M. J., & Jacob, K. S. (2009) · Indian Journal of Psychiatry · doi:10.4103/0019-5545.44905 · Cited by 111 · see citing works
A critical analysis of the ‘amyloid cascade hypothesis’
A. Armstrong, R. (2014) · Folia Neuropathologica · doi:10.5114/fn.2014.45562 · Cited by 110 · see citing works
Alzheimer's disease: The amyloid hypothesis on trial
Harrison, J. R., & Owen, M. J. (2016) · The British Journal of Psychiatry · doi:10.1192/bjp.bp.115.167569 · Cited by 96 · see citing works
Abushouk, A. I., Elmaraezy, A., Aglan, A. D., Salama, R., Fouda, S., Fouda, R., & AlSafadi, A. M. (2017) · BMC Neurology · doi:10.1186/s12883-017-0850-1 · Cited by 86 · see citing works
Normal cognition in transgenic BRI2-Aβ mice
Kim, J., Chakrabarty, P., Hanna, A., March, A., Dickson, D. W., Borchelt, D. R., Golde, T., & Janus, C. (2013) · Molecular Neurodegeneration · doi:10.1186/1750-1326-8-15 · Cited by 83 · see citing works
Ten Challenges of the Amyloid Hypothesis of Alzheimer’s Disease
Kepp, K. P. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160550 · Cited by 80 · see citing works
Rygiel, K. (2016) · Indian Journal of Pharmacology · doi:10.4103/0253-7613.194867 · Cited by 74 · see citing works
Alzheimer amyloid hypothesis lives on
Mullard, A. (2016) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2016.281 · Cited by 70 · see citing works
Tesi, N., van der Lee, S. J., Hulsman, M., Jansen, I. E., Stringa, N., van Schoor, N. M., Scheltens, P., van der Flier, W. M., Huisman, M., Reinders, M. J. T., et al. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-01018-7 · Cited by 67 · see citing works
β-Amyloid Induces Pathology-Related Patterns of Tau Hyperphosphorylation at Synaptic Terminals
Wu, H., Kuo, P.-C., Wang, Y.-T., Lin, H.-T., Roe, A. D., Wang, B. Y., Han, C., Hyman, B. T., Chen, Y., & Tai, H. (2018) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nly059 · Cited by 66 · see citing works
Three FDA advisory panel members resign over approval of Alzheimer’s drug
Mahase, E. (2021) · BMJ · doi:10.1136/bmj.n1503 · Cited by 48 · see citing works
Promising Targets for the Treatment of Neurodegenerative Diseases
Haeberlein, S. B., & Harris, T. (2015) · Clinical Pharmacology & Therapeutics · doi:10.1002/cpt.195 · Cited by 35 · see citing works
Watson, J., Saunders, S., Terrera, G. M., Ritchie, C. W., Evans, A., Luz, S. F., & Clarke, C. L. (2019) · Health Expectations · doi:10.1111/hex.12876 · Cited by 31 · see citing works
Overview of dominantly inherited AD and top‐line DIAN‐TU results of solanezumab and gantenerumab
Bateman, R. J., Aschenbrenner, A. J., Benzinger, T. L. S., Clifford, D. B., Coalier, K. A., Cruchaga, C., Fagan, A. M., Farlow, M. R., Goate, A., Gordon, B. A., et al. (2020) · Alzheimer s & Dementia · doi:10.1002/alz.041129 · Cited by 5 · see citing works
Flagged first, then by citations
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Sorted by citations
Role of Aducanumab in the Treatment of Alzheimer’s Disease: Challenges and Opportunities
Vaz, M., Silva, V., Monteiro, C., & Silvestre, S. (2022) · Clinical Interventions in Aging · doi:10.2147/cia.s325026 · Cited by 183 · see citing works
“Thirdly, the close collaboration between the FDA and the sponsor could have impacted the objectivity of the FDA’s decision.(63,64) Furthermore, the AD ́s advocacy groups exerted much pressure on the FDA, defending that a marginal benefit of aducanumab would be significant to patients and caregivers.”
BackgroundYan, L., Guo, M.-S., Zhang, Y., Yu, L., Wu, J.-M., Tang, Y., Ai, W., Zhu, F.-D., Law, B. Y.-K., Chen, Q., et al. (2022) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2022/5288698 · Cited by 97 · see citing works
Pathophysiology of Alzheimer’s Disease
Yarns, B. C., Holiday, K. A., Carlson, D. M., Cosgrove, C. K., & Melrose, R. J. (2022) · Psychiatric Clinics of North America · doi:10.1016/j.psc.2022.07.003 · Cited by 68 · see citing works
Drug repurposing for Alzheimer’s disease from 2012–2022—a 10-year literature review
Grabowska, M. E., Huang, A., Wen, Z., Li, B., & Wei, W.-Q. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1257700 · Cited by 55 · see citing works
“From 2003 to 2022, only one new drug, aducanumab, was controversially approved for use in AD (Mukhopadhyay and Banerjee, 2021).”
BackgroundRecent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
Thawabteh, A. M., Ghanem, A. W., AbuMadi, S., Thaher, D., Jaghama, W., Karaman, D., & Karaman, R. (2024) · Molecules · doi:10.3390/molecules29215131 · Cited by 56 · see citing works
“In spite of this, the FDA granted expedited approval on the grounds of the EMERGE trial’s documented decrease in amyloid levels [132,185–187].”
Background“Aducanumab” making a comeback in Alzheimer’s disease: An old wine in a new bottle
Behl, T., Kaur, I., Sehgal, A., Singh, S., Sharma, N., Makeen, H. A., Albratty, M., Alhazmi, H. A., Felemban, S. G., Alsubayiel, A. M., et al. (2022) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2022.112746 · Cited by 50 · see citing works
What have we learnt from past failures in Alzheimer’s disease drug discovery?
Cacabelos, R. (2022) · Expert Opinion on Drug Discovery · doi:10.1080/17460441.2022.2033724 · Cited by 22 · see citing works
West, M., Cheng, Y., He, Y., Leng, Y., Magdamo, C., Hyman, B. T., Dickson, J. R., Serrano-Pozo, A., Blacker, D., & Das, S. (2025) · JMIR Aging · doi:10.2196/65178 · Cited by 8 · see citing works
- Authors
- Mukhopadhyay, S., & Banerjee, D.
- Affiliations
- National Institute of Mental Health and Neurosciences (IN)
- Corresponding author
- Banerjee, Debanjan
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2021-10-12
- Volume
- 83
- Issue
- 4
- Pages
- 1537-1552
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W3191310544
- Cited by
- 66
- References
- 68
- Citations by year
- 2026: 7 · 2025: 6 · 2024: 8 · 2023: 12 · 2022: 28 · 2021: 5
- FWCI
- 1.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- 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
- aducanumab, Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Brain, Humans, United States, United States Food and Drug Administration, Amyloid beta-Peptides, Drug Approval, Antibodies, Monoclonal, Humanized
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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