The DOI matches its Crossref record; 97 of the 97 references it cites were found in a registry or an index.
Impact of Anti-amyloid-β Monoclonal Antibodies on the Pathology and Clinical Profile of Alzheimer’s Disease: A Focus on Aducanumab and Lecanemab
Open accessAbstract
Alzheimer’s disease (AD) is the most prevalent form of age-related dementia in the world, and its main pathological features consist of amyloid-β (Aβ) plaque deposits and neurofibrillary tangles formed by hyperphosphorylated tau protein. So far, only a few AD treatments approved have been applied in the clinic, but the effects of these drugs are limited only for partial symptomatic relief to patients with AD and are unable to alter AD progression. Later, all efforts for AD treatments with targeting the pathogenic factors were unsuccessful over the past decades, which suggested that the pathogenesis of AD is complex. Recently, disease-modifying therapies (DMTs) that can change the underlying pathophysiology of AD, with anti-Aβ monoclonal antibodies (mabs) (e.g., aducanumab, bapineuzumab, gantenerumab, solanezumab, and lecanemab) have been developed successively and conducted in clinical trials based on the theory that a systemic failure of cell-mediated Aβ clearance contributes to AD occurrence and progression. In the review, we summarized recent studies on the therapeutic effects and clinical trial results of these mabs in patients with AD. Specifically, we focused on the discussion of the impact of aducanumab and lecanemab on AD pathology and clinical profiles. The review provides a possible evidence for applying immunotherapy with anti-Aβ mabs in AD and analyzes lessons learned from these clinical trials in order to further study the therapeutic and adverse effects of these anti-Aβ mabs on AD.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
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 Shi et al. 2022
In the citing paper
“Studies have shown that Aβ buildup can start 15–20 years before clinical symptoms appear, indicating that therapy effectiveness may depend on early intervention [88,89].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [89]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Aducanumab Use in Symptomatic Alzheimer Disease Evidence in Focus [RETIRED]
Day, G. S., Scarmeas, N., Dubinsky, R., Coerver, K., Mostacero, A., West, B., Wessels, S. R., & Armstrong, M. J. (2022) · Neurology · doi:10.1212/wnl.0000000000200176 · Cited by 42
RetractedClinical and biomarker changes in dominantly inherited Alzheimer's disease
Bateman, R. J., Xiong, C., Benzinger, T. L. S., Fagan, A. M., Goate, A., Fox, N. C., Marcus, D. S., Cairns, N. J., Xie, X., Blazey, T. M., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1202753 · Cited by 3,814
Neuropathological alterations in Alzheimer disease
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006189 · Cited by 3,345
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
Bloom (2014) · doi:10.1001/jamaneurol.2013.5847 · Cited by 2,194
Cerebrospinal fluid and plasma biomarkers in Alzheimer disease
Blennow, K., Hampel, H., Weiner, M., & Zetterberg, H. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.4 · Cited by 1,863
Masters, C. L., Bateman, R., Blennow, K., Rowe, C. C., Sperling, R. A., & Cummings, J. L. (2015) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2015.56 · Cited by 1,853
Phase 3 Trials of Solanezumab for Mild-to-Moderate Alzheimer's Disease
Doody, R. S., Thomas, R. G., Farlow, M., Iwatsubo, T., Vellas, B., Joffe, S., Kieburtz, K., Raman, R., Sun, X., Aisen, P. S., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1312889 · Cited by 1,668
DeMattos, R. B., Bales, K. R., Cummins, D. J., Dodart, J.-C., Paul, S. M., & Holtzman, D. M. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.151261398 · Cited by 1,298
Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ 42 in humans
Fagan, A. M., Mintun, M. A., Mach, R. H., Lee, S., Dence, C. S., Shah, A. R., LaRossa, G. N., Spinner, M. L., Klunk, W. E., Mathis, C. A., et al. (2006) · Annals of Neurology · doi:10.1002/ana.20730 · Cited by 1,246
Research works printed but not linked: 3
- 221AD301 Phase 3 Study of Aducanumab (BIIB037) in Early Alzheimer’s Disease (ENGAGE).
- 221AD302 Phase 3 Study of Aducanumab (BIIB037) in Early Alzheimer’s Disease (EMERGE).
- Swanson, 2018, Clinical and biomarker updates from BAN2401 Study 201 in early AD, Proceedings of Clinical Trials on Alzheimer’s Disease Conference
Cited by
Sorted by citations
Multifunctional nanoparticle-mediated combining therapy for human diseases
Li, X., Peng, X., Zoulikha, M., Boafo, G. F., Magar, K. T., Ju, Y., & He, W. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01668-1 · Cited by 573
McDade, E., Cummings, J. L., Dhadda, S., Swanson, C. J., Reyderman, L., Kanekiyo, M., Koyama, A., Irizarry, M. C., Kramer, L. D., & Bateman, R. J. (2022) · Alzheimer s Research & Therapy · doi:10.1186/s13195-022-01124-2 · Cited by 328
Oxidative stress in Alzheimer’s disease: current knowledge of signaling pathways and therapeutics
Dhapola, R., Beura, S. K., Sharma, P., Singh, S. K., & HariKrishnaReddy, D. (2024) · Molecular Biology Reports · doi:10.1007/s11033-023-09021-z · Cited by 288
Singh, B., Day, C. M., Abdella, S., & Garg, S. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.01.047 · Cited by 256
Human Microglia Show Unique Transcriptional Changes in Alzheimer's Disease
Prater, K. E., Green, K. J., Mamde, S., Sun, W., Cochoit, A., Smith, C. L., Chiou, K. L., Heath, L., Rose, S. E., Wiley, J., et al. (2023) · Nature Aging · doi:10.1038/s43587-023-00424-y · Cited by 164
Metadata
- Authors
- Shi, M., Chu, F., Zhu, F., & Zhu, J.
- Affiliations
- First Hospital of Jilin University (CN)
- Shenzhen University (CN)
- Karolinska University Hospital (SE)
- Corresponding author
- Zhu, Feiqi
- Zhu, Jie
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2022-04-12
- Volume
- 14
- Pages
- 870517-870517
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC9039457
- OpenAlex
- W4223533048
- Cited by
- 275
- References
- 97
- Citations by year
- 2026: 28 · 2025: 66 · 2024: 104 · 2023: 68 · 2022: 8
- FWCI
- 8.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- People's Government of Jilin Province
- Jilin University
- Sanming Project of Medicine in Shenzhen (SZSM201801014)
- First Hospital of Jilin University
- 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
- Alzheimer's disease, anti-amyloid beta monoclonal antibody, aducanumab, lecanemab, amyloid plaques, disease-modifying therapy, immunotherapy, clinical trial results, adverse effects, amyloid-beta clearance, tau hyperphosphorylation, neurofibrillary tangles
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 ›
Are you an author, or do you see a problem with this page? Request a review
