Current thinking on the mechanistic basis of Alzheimer's and implications for drug development
Abstract
Alzheimer disease (AD) is the most common cause of dementia and is characterized by the aggregation and accumulation of two proteins in the brain, amyloid‐β (Aβ) and tau. Aβ and tau begin to buildup 15‐20 years before the clinical onset of AD dementia. Increasing evidence suggests that preventing or decreasing the amount of aggregated forms of both Aβ and tau in the brain can serve as potential disease‐modifying treatments for AD.
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Single chain fragment variables derived from an anti-tau antibody decreased p-tau accumulation in the brain of PS19 tau transgenic mice, indicating that microglial activation via the Fc domain of an antibody is not required for the protective effect.
“A recent paper also showed that single chain fragment variables (scFvs) derived from an anti-tau antibody decreased p-tau accumulation in the brain of PS19 tau transgenic mice indicating that microglial activation via the Fc domain of an antibody is not required for the protective effect of such a treatment [185].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [185]
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- Authors
- Ising, C., Stanley, M., & Holtzman, D.
- Affiliations
- Washington University in St. Louis (US)
- Department of Neurology Hope Center for Neurological Disorders, Charles F and Joanne Knight Alzheimer's Disease Research Center, Washington University School of Medicine St. Louis Missouri USA
- ORCID
- Venue
- Clinical Pharmacology & Therapeutics
- Publisher
- Wiley
- Published
- 2015-09-10
- Volume
- 98
- Issue
- 5
- Pages
- 469-471
- ISSN
- 0009-9236 (ISSN-L)
- 1532-6535
- OpenAlex
- W1860832468
- Cited by
- 59
- References
- 5
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 1 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 5 · 2018: 10 · 2017: 14 · 2016: 7 · 2015: 2
- FWCI
- 8.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Pharmacology & Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- The JPB Foundation and Cure Alzheimer's Fund
- National Science Foundation graduate research fellowship (DGE-1143954)
- 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, amyloid-beta, tau protein, protein aggregation, disease-modifying therapy, drug development, dementia, preclinical disease
- MeSH terms
- Alzheimer Disease, Brain, Humans, Immunotherapy, Thinking, Amyloid beta-Peptides, tau Proteins, Drug Discovery
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