Antibody engineering for optimized immunotherapy in Alzheimer's disease
Antibody engineering for optimized immunotherapy in Alzheimer's disease
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.
Alzheimers disease, Amyloid, Antibody engineering, Immunotherapy, Neuroinflammation
1-12
Sumner, Isabelle L.
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Edwards, Ross A.
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Asuni, Ayodeji A.
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Teeling, Jessica L.
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Sumner, Isabelle L.
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Edwards, Ross A.
564476aa-0492-46e5-9f1e-7f5d77d522a1
Asuni, Ayodeji A.
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Teeling, Jessica L.
fcde1c8e-e5f8-4747-9f3a-6bdb5cd87d0a
Sumner, Isabelle L., Edwards, Ross A., Asuni, Ayodeji A. and Teeling, Jessica L.
(2018)
Antibody engineering for optimized immunotherapy in Alzheimer's disease.
Frontiers in Neuroscience, 12 (APR), , [254].
(doi:10.3389/fnins.2018.00254).
Abstract
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.
Text
fnins-12-00254
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Accepted/In Press date: 3 April 2018
e-pub ahead of print date: 23 April 2018
Keywords:
Alzheimers disease, Amyloid, Antibody engineering, Immunotherapy, Neuroinflammation
Identifiers
Local EPrints ID: 422418
URI: http://eprints.soton.ac.uk/id/eprint/422418
ISSN: 1662-4548
PURE UUID: 61e8f45f-8183-47be-9a5c-48efce3b9aff
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Date deposited: 23 Jul 2018 16:31
Last modified: 06 Jun 2024 01:42
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Contributors
Author:
Isabelle L. Sumner
Author:
Ross A. Edwards
Author:
Ayodeji A. Asuni
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