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Cited by 95Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

Interleukins, Inflammation, and Mechanisms of Alzheimer's Disease

Weisman, David, Hakimian, Edwin, Ho, Gilbert J.·2006·Vitamins & Hormones
DOI 10.1016/s0083-6729(06)74020-1
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Abstract

Alzheimer's disease (AD) is the most common progressive neurodegenerative form of dementia in the elderly and is characterized neuropathologically by neurofibrillary tangles (NFT), amyloid neuritic plaques (NP), and prominent synaptic and eventually neuronal loss. Although the molecular basis of AD is not clearly understood, a neuroinflammatory process, triggered by Abeta42, plays a central role in the neurodegenerative process. This inflammatory process is driven by activated microglia, astrocytes and the induction of proinflammatory molecules and related signaling pathways, leading to both synaptic and neuronal damage as well as further inflammatory cell activation. Epidemiologic data as well as clinical trial evidence suggest that nonsteroidal anti-inflammatory drug (NSAID) use may decrease the incidence of AD, further supporting a role for inflammation in AD pathogenesis. Although the precise molecular and cellular relationship between AD and inflammation remains unclear, interleukins and cytokines might induce activation of signaling pathways leading to futher inflammation and neuronal injury. This chapter will discuss the association between interleukins and neurodegeneration in AD and highlight the significance of genetic and clinical aspects of interleukins in disease expression and progression. As part of an emerging inflammatory signaling network underlying AD pathogenesis, beta-amyloid (Abeta) stimulates the glial and microglial production of interleukins and other cytokines, leading to an ongoing inflammatory cascade and contributing to synaptic dysfunction and loss, and later, neuronal death. Inflammatory pathways involving interleukin and cytokine signaling might suggest potential targets for intervention and influence the development of novel therapies to circumvent synaptic and neuronal dysfunction ultimately leading to AD neurodegeneration.

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Crossref · 10.1016/s0083-6729(06)74020-1

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131 of 131 references verified0 citation errors · 0 not checkable

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  • Anti-inflammatory molecules like IL-4 and IL-10 may antagonize the proinflammatory effects of IL-1β and IL-6.

    “Meanwhile, anti-inflammatory molecules like IL-4 and IL-10 may antagonize the proinflammatory effects of IL-1β and IL-6 [103].”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [103]

  • Interleukins such as IL-18, IL-34, IL-4, IL-10, IL-13, and others have been reported as either up- or downregulated in patient brain tissue, CSF or blood in AD and related tauopathies.

    “Interleukins such as IL-18, IL-34, IL-4, IL-10 IL-13, and others have been reported as either up or downregulated in patient brain tissue, CSF or blood [92, 103, 167].”

    From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [103]

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Authors
Weisman, D., Hakimian, E., & Ho, G. J.
Affiliations
  • United States Department of Veterans Affairs (US)
  • University of California San Diego (US)
ORCID
Ho, Gilbert J.
Venue
Vitamins & Hormones
Publisher
Elsevier
Published
2006
Volume
74
Pages
505-530
ISSN
0083-6729 (ISSN-L)
DOI
10.1016/s0083-6729(06)74020-1
OpenAlex
W1484591758
Cited by
95
References
138
Citations by year
2026: 2 · 2025: 3 · 2024: 2 · 2023: 7 · 2022: 3 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 6 · 2016: 7 · 2015: 5 · 2014: 5 · 2013: 2 · 2012: 6
FWCI
19.56
Type
book chapter
Language
en
Open access
closed
Locations
  • Vitamins and hormones (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, neuroinflammation, interleukins, cytokines, amyloid-beta, microglia, astrocytes, neurodegeneration, synaptic dysfunction, neuronal cell death, nonsteroidal anti-inflammatory drugs, neurofibrillary tangles, amyloid plaques, inflammatory signaling
MeSH terms
Alzheimer Disease, Animals, Brain, Humans, Inflammation, Interleukins, Inflammation Mediators, Mice, Rats

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