The DOI matches its Crossref record; 225 of the 225 references it cites were found in a registry or an index.
The dendritic hypothesis for Alzheimer's disease pathophysiology
Open accessAbstract
Converging evidence indicates that processes occurring in and around neuronal dendrites are central to the pathogenesis of Alzheimer's disease. These data support the concept of a "dendritic hypothesis" of AD, closely related to the existing synaptic hypothesis. Here we detail dendritic neuropathology in the disease and examine how Aβ, tau, and AD genetic risk factors affect dendritic structure and function. Finally, we consider potential mechanisms by which these key drivers could affect dendritic integrity and disease progression. These dendritic mechanisms serve as a framework for therapeutic target identification and for efforts to develop disease-modifying therapeutics for Alzheimer's disease.
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“Aβ, tau, and AD genetic risk factors affect dendritic integrity and disease progression [14].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [14]
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2 retracted
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Cited by
Sorted by citations
Roles of tau protein in health and disease
Guo, T., Noble, W., & Hanger, D. P. (2017) · Acta Neuropathologica · doi:10.1007/s00401-017-1707-9 · Cited by 1,003
Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease
Khan, S., Barve, K. H., & Kumar, M. S. (2020) · Current Neuropharmacology · doi:10.2174/1570159x18666200528142429 · Cited by 820
“Aβ, tau, and AD genetic risk factors affect dendritic integrity and disease progression [14].”
BackgroundCurrent Research Therapeutic Strategies for Alzheimer’s Disease Treatment
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Masitinib for the treatment of mild to moderate Alzheimer’s disease
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Metadata
- Authors
- Cochran, J. N., Hall, A. M., & Roberson, E. D.
- Affiliations
- University of Alabama at Birmingham (US)
- Corresponding author
- Roberson, Erik D.
- Venue
- Brain Research Bulletin
- Publisher
- Elsevier BV
- Published
- 2014-04
- Volume
- 103
- Pages
- 18-28
- ISSN
- 0361-9230 (ISSN-L)
- PMC
- PMC3989444
- OpenAlex
- W2046296412
- Cited by
- 114
- References
- 225
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 13 · 2023: 10 · 2022: 9 · 2021: 12 · 2020: 13 · 2019: 5 · 2018: 6 · 2017: 13 · 2016: 9 · 2015: 12 · 2014: 4
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research Bulletin (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of General Medical Sciences (T32GM008111)
- National Institute of Neurological Disorders and Stroke (R01NS075487, T32NS061788)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, dendrites, amyloid-beta, tau protein, genetic risk factors, disease-modifying therapy, therapeutic target
- MeSH terms
- Alzheimer Disease, Animals, Dendrites, Humans, Amyloid beta-Peptides, Neurites, Tauopathies
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