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.
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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 Shi et al. 2022
Aβ buildup can start 15-20 years before clinical symptoms appear, indicating therapy effectiveness may depend on early intervention.
“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]
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- 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 · 2021: 1
- 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
- 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
- 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
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