The DOI matches its Crossref record; 115 of the 115 references it cites were found in a registry or an index.
Tumour Necrosis Factor Modulation for Treatment of Alzheimerʼs Disease: Rationale and Current Evidence
Abstract
Tumour necrosis factor (TNF), a key regulator of varied physiological mechanisms in multiple organ systems, is an immune signalling molecule produced by glia, neurons, macrophages and other immune cells. In the brain, among other functions, TNF serves as a gliotransmitter, secreted by glial cells that envelope and surround synapses, which regulates synaptic communication between neurons. The role of TNF as a gliotransmitter may help explain the profound synaptic effects of TNF that have been demonstrated in the hippocampus, in the spinal cord and in a variety of experimental models. Excess TNF is present in the CSF of individuals with Alzheimer's disease (AD), and has been implicated as a mediator of the synaptic dysfunction that is hypothesized to play a central role in the pathogenesis of AD. TNF may also play a role in endothelial and microvascular dysfunction in AD, and in amyloidogenesis and amyloid-induced memory dysfunction in AD. Genetic and epidemiological evidence has implicated increased TNF production as a risk factor for AD. Perispinal administration of etanercept, a potent anti-TNF fusion protein, produced sustained clinical improvement in a 6-month, open-label pilot study in patients with AD ranging from mild to severe. Subsequent case studies have documented rapid clinical improvement following perispinal etanercept in both AD and primary progressive aphasia, providing evidence of rapidly reversible, TNF-dependent, pathophysiological mechanisms in AD and related disorders. Perispinal etanercept for AD merits further study in randomized clinical trials.
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“TNF-α has two primary receptors, TNFR1 which is constitutively expressed throughout the brain and TNFR2 which is inducible and primarily localized to glial and endothelial cells [141].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [141]
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Cites
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Cited by
Sorted by citations
Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease.
(2015) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2305-5839.2015.03.49 · Cited by 1,288
Glial contributions to neurodegeneration in tauopathies
Leyns, C. E. G., & Holtzman, D. M. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0192-x · Cited by 409
RETRACTED: Neuroinflammatory Markers: Key Indicators in the Pathology of Neurodegenerative Diseases
Rauf, A., Badoni, H., Abu‐Izneid, T., Olatunde, A., Rahman, M. M., Painuli, S., Semwal, P., Wilairatana, P., & Mubarak, M. S. (2022) · Molecules · doi:10.3390/molecules27103194 · Cited by 316
RetractedRole of inflammatory molecules in the Alzheimer's disease progression and diagnosis
Bagyinszky, E., Giau, V. V., Shim, K., Suk, K., An, S. S. A., & Kim, S. (2017) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2017.03.031 · Cited by 276
TNFα in synaptic function: switching gears
Santello, M., & Volterra, A. (2012) · Trends in Neurosciences · doi:10.1016/j.tins.2012.06.001 · Cited by 253
Metadata
- Authors
- Tobinick, E.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Tobinick, Edward
- ORCID
- Tobinick, Edward
- Venue
- CNS Drugs
- Published
- 2009-09
- Volume
- 23
- Issue
- 9
- Pages
- 713-725
- ISSN
- 1172-7047 (ISSN-L)
- OpenAlex
- W2053730308
- Cited by
- 117
- References
- 115
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 7 · 2019: 6 · 2018: 8 · 2017: 9 · 2016: 5 · 2015: 11 · 2014: 9 · 2013: 10 · 2012: 11
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- CNS Drugs (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- TNF-α, Alzheimer's disease, etanercept, anti-TNF therapy, gliotransmitters, synaptic dysfunction, amyloidogenesis, microvascular dysfunction, primary progressive aphasia
- MeSH terms
- Etanercept, Alzheimer Disease, Animals, Brain, Humans, Immunoglobulin G, Synaptic Transmission, Risk Factors, Tumor Necrosis Factor-alpha, Drug Delivery Systems, Receptors, Tumor Necrosis Factor
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