Cited by 61Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Current thinking on the mechanistic basis of Alzheimer's and implications for drug development

Ising, C, Stanley, M, Holtzman, DM·2015·Clinical Pharmacology & Therapeutics

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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Crossref · 10.1002/cpt.200

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5 of 5 references verified0 citation errors · 0 not checkable

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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
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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