Inflammatory Cytokines and Alzheimer’s Disease: A Review from the Perspective of Genetic Polymorphisms
Open accessAbstract
Neuroinflammatory processes are a central feature of Alzheimer's disease (AD) in which microglia are over-activated, resulting in the increased production of pro-inflammatory cytokines. Moreover, deficiencies in the anti-inflammatory system may also contribute to neuroinflammation. Recently, advanced methods for the analysis of genetic polymorphisms have further supported the relationship between neuroinflammatory factors and AD risk because a series of polymorphisms in inflammation-related genes have been shown to be associated with AD. In this review, we summarize the polymorphisms of both pro- and anti-inflammatory cytokines related to AD, primarily interleukin-1 (IL-1), IL-6, tumor necrosis factor alpha, IL-4, IL-10, and transforming growth factor beta, as well as their functional activity in AD pathology. Exploration of the relationship between inflammatory cytokine polymorphisms and AD risk may facilitate our understanding of AD pathogenesis and contribute to improved treatment strategies.
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Treatment options for neuroinflammation associated with AD have been investigated, including IL-1β antagonists such as canakinumab.
“Treatment options for neuroinflammation associated with AD have been investigated, including IL-1β antagonists such as canakinumab [206,207,208].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [208]
Cholinesterase inhibitors and NMDA receptor antagonists are the only two categories of medications prescribed to address AD symptoms.
“Cholinesterase inhibitors and NMDA receptor antagonists are the only two categories of medications that are prescribed to address symptoms [208].”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [208]
Research on cytokine inhibition has focused on anti-inflammatory medications that interact with pro-inflammatory cytokines such as TNF-a and IL-1 beta.
“Research on cytokine inhibition has focused on anti-inflammatory medications that interact with pro-inflammatory cytokines such as TNF-a and IL-1 beta.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [208]
The decline in cognitive abilities in AD is positively correlated with the breakdown of synaptic connections.
“Regarding the plasticity of synapses and neurodefense, it has been found that the decline in cognitive abilities in ADs is positively correlated with the breakdown of synaptic connections.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [208]
Neurotransmitter modulation is useful for AD.
“Consequently, neurotransmitter modulation is useful.”
From Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease (2024) · cites this paper as [208]
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Trends in insulin resistance: insights into mechanisms and therapeutic strategy
Li, M., Chi, X., Wang, Y., Setrerrahmane, S., Xie, W., & Xu, H. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01073-0 · Cited by 939 · see citing works
Neuroinflammation in Alzheimer’s Disease: Current Progress in Molecular Signaling and Therapeutics
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Recent Advances in Therapeutics for the Treatment of Alzheimer’s Disease
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“Cholinesterase inhibitors and NMDA receptor antagonists are the only two categories of medications that are prescribed to address symptoms [208].”
BackgroundCerebrospinal Fluid Levels of Interleukin-8 in Delirium, Dementia, and Cognitively Healthy Patients
Sajjad, M. U., Blennow, K., Knapskog, A. B., Idland, A.-V., Chaudhry, F. A., Wyller, T. B., Zetterberg, H., & Watne, L. O. (2020) · Journal of Alzheimer’s Disease · doi:10.3233/jad-190941 · Cited by 34 · see citing works
- Authors
- Su, F., Bai, F., & Zhang, Z.
- Affiliations
- Zhongda Hospital Southeast University (CN)
- Corresponding author
- Bai, Feng
- Venue
- Neuroscience Bulletin
- Published
- 2016-08-27
- Volume
- 32
- Issue
- 5
- Pages
- 469-480
- ISSN
- 1995-8218 (ISSN-L)
- 1673-7067
- PMC
- PMC5563762
- OpenAlex
- W2508044717
- Cited by
- 221
- References
- 145
- Citations by year
- 2026: 5 · 2025: 26 · 2024: 24 · 2023: 25 · 2022: 21 · 2021: 33 · 2020: 31 · 2019: 26 · 2018: 16 · 2017: 13 · 2016: 1
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuroscience Bulletin (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81201080, 863 Program, 91332104, NCET-13)
- Ministry of Education of the People's Republic of China
- Government of Jiangsu Province (BL2013025)
- Natural Science Foundation of Jiangsu Province (BK2012337)
- Program for New Century Excellent Talents in University (NCET-13-0117, NCET-13)
- National High-tech Research and Development Program
- 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, inflammatory cytokines, anti-inflammatory cytokines, genetic polymorphism, microglial activation, interleukin-1, interleukin-6, TNF-α, IL-4, IL-10, TGF-beta, disease risk, AD pathogenesis
- MeSH terms
- Alzheimer Disease, Animals, Humans, Cytokines, Polymorphism, Single Nucleotide
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