Amyloid‐β immunotherapy for alzheimer disease: Is it now a long shot?
Abstract
The amyloid‐β (Aβ) cascade hypothesis of Alzheimer disease (AD) holds that brain accumulation of Aβ initiates the disease process. Accordingly, drug research has targeted Aβ production, clearance, and deposition as therapeutic strategies. Unfortunately, candidate drugs have failed to show clinical benefit in established, early, or prodromal disease, or in those with high AD risk. Currently, monoclonal antibodies specifically directed against the most neurotoxic Aβ forms are undergoing large‐scale trials to confirm initially encouraging results. However, recent findings on the normal physiology of Aβ suggest that accumulation may be compensatory rather than the pathological initiator. If this is true, alternative strategies will be needed to defeat this devastating disease. ANN NEUROL 2019;85:303–315.
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Other Aβ immunotherapy mechanisms include a direct method in which Aβ plaques are unbundled and a peripheral sink mechanism removing Aβ from the brain to plasma.
“There are several other mechanisms like direct method (in which Aβ plaque are unbundled) and peripheral sink mechanism (removal of Aβ from the brain to plasma) [118].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [118]
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Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease
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- Authors
- Panza, F., Lozupone, M., Seripa, D., & Imbimbo, B. P.
- Affiliations
- Casa Sollievo della Sofferenza (IT)
- University of Bari Aldo Moro (IT)
- Chiesi (Italy) (IT)
- Corresponding author
- Panza, Francesco
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2019-01-28
- Volume
- 85
- Issue
- 3
- Pages
- 303-315
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2909242954
- Cited by
- 178
- References
- 120
- Citations by year
- 2026: 16 · 2025: 11 · 2024: 23 · 2023: 19 · 2022: 25 · 2021: 31 · 2020: 35 · 2019: 17
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Biogen
- Genentech
- 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
- amyloid-beta, Alzheimer's disease, immunotherapy, amyloid hypothesis, monoclonal antibodies, amyloid-beta clearance, clinical trials, prodromal Alzheimer's disease
- MeSH terms
- Drug Development, Alzheimer Disease, Antibodies, Monoclonal, Brain, Humans, Immunotherapy, Amyloid beta-Peptides, Molecular Targeted Therapy
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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.
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