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Review
, 32 (5), 469-80

Inflammatory Cytokines and Alzheimer's Disease: A Review From the Perspective of Genetic Polymorphisms

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Review

Inflammatory Cytokines and Alzheimer's Disease: A Review From the Perspective of Genetic Polymorphisms

Fan Su et al. Neurosci Bull.

Abstract

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.

Keywords: Alzheimer’s disease; Cytokine; Genetic polymorphism; Neuroinflammation.

Figures

Fig. 1
Fig. 1
Involvement of microglia in AD development. AD-related pathology induces chronic activation of microglia, exacerbating neuroinflammation and inhibiting the clearance of Aβ, in turn leading to AD-related deterioration.

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