Antibody Engineering for Optimized Immunotherapy in Alzheimer's Disease
Open accessAbstract
There are nearly 50 million people with Alzheimer's disease (AD) worldwide and currently no disease modifying treatment is available. AD is characterized by deposits of Amyloid-β (Aβ), neurofibrillary tangles, and neuroinflammation, and several drug discovery programmes studies have focussed on Aβ as therapeutic target. Active immunization and passive immunization against Aβ leads to the clearance of deposits in humans and transgenic mice expressing human Aβ but have failed to improve memory loss. This review will discuss the possible explanations for the lack of efficacy of Aβ immunotherapy, including the role of a pro-inflammatory response and subsequent vascular side effects, the binding site of therapeutic antibodies and the timing of the treatment. We further discuss how antibodies can be engineered for improved efficacy.
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Second-generation antibodies have low binding activity at Fcγ regions, which are mainly involved in side effects of first-line monoclonal antibodies.
“These antibodies are mainly engineered and have low binding activity at Fcγ regions which are mainly involved in side effects of first line monoclonal antibodies [121].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [121]
Second-generation engineered antibodies including BAN2401, SAR255952 and Aducanumab are in development for Alzheimer's disease.
“Various engineered antibodies or second-generation antibodies are in the development phase. It includes BAN2401 (that selectively binds to large soluble Aβ protofibrils), SAR255952 (which primarily targets soluble protofibrillar and fibrillar species of Aβ), Aducanumab (which binds to the N-terminus of Aβ3-6), etc.”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [121]
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References 109 · Cited by 24
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- lu080 · DOI · Paper page
- Authors
- Sumner, I. L., Edwards, R. A., Asuni, A. A., & Teeling, J. L.
- Affiliations
- University of Southampton (GB)
- Lundbeck (Denmark) (DK)
- Corresponding author
- Teeling, Jessica L.
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2018-04-23
- Volume
- 12
- Pages
- 254-254
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC5924811
- OpenAlex
- W2799675696
- Cited by
- 24
- References
- 109
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 6 · 2021: 1 · 2020: 5 · 2019: 4 · 2018: 1
- FWCI
- 0.36
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Monoclonal and Polyclonal Antibodies Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, antibody engineering, amyloid-beta immunotherapy, active immunization, passive immunization, anti-amyloid antibodies, neuroinflammation, antibody binding sites, treatment timing, transgenic mouse model, disease-modifying therapy
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