Cited by 352Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

Microglia in the Neuroinflammatory Pathogenesis of Alzheimer’s Disease and Related Therapeutic Targets

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Cai, Yongle, Liu, Jingliu, Wang, Bin, Sun, Miao, Yang, Hao·2022·Frontiers in Immunology

Abstract

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease worldwide, characterized by progressive neuron degeneration or loss due to excessive accumulation of β-amyloid (Aβ) peptides, formation of neurofibrillary tangles (NFTs), and hyperphosphorylated tau. The treatment of AD has been only partially successful as the majority of the pharmacotherapies on the market may alleviate some of the symptoms. In the occurrence of AD, increasing attention has been paid to neurodegeneration, while the resident glial cells, like microglia are also observed. Microglia, a kind of crucial glial cells associated with the innate immune response, functions as double-edge sword role in CNS. They exert a beneficial or detrimental influence on the adjacent neurons through secretion of both pro-inflammatory cytokines as well as neurotrophic factors. In addition, their endocytosis of debris and toxic protein like Aβ and tau ensures homeostasis of the neuronal microenvironment. In this review, we will systematically summarize recent research regarding the roles of microglia in AD pathology and latest microglia-associated therapeutic targets mainly including pro-inflammatory genes, anti-inflammatory genes and phagocytosis at length, some of which are contradictory and controversial and warrant to further be investigated.

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Crossref · 10.3389/fimmu.2022.856376

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  • Microglia may help contain amyloid plaques, phagocytose pathological material, support synapses, and limit inflammatory spread; yet they may also release pro-inflammatory mediators, promote complement-associated synapse loss, propagate neurotoxic signaling, and contribute to chronic tissue damage.

    “Microglia may help contain amyloid plaques, phagocytose pathological material, support synapses, and limit inflammatory spread; yet they may also release pro-inflammatory mediators, promote complement-associated synapse loss, propagate neurotoxic signaling, and contribute to chronic tissue damage.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [19]

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  • The same broad category of microglial activation can describe processes with opposite biological consequences.

    “The central unresolved issue is that the same broad category of “microglial activation” can describe processes with opposite biological consequences.”
  • Alzheimer's neuroinflammation is a dynamic balance between protective and harmful microglial programs, with disease stage and local tissue environment determining whether immune activation is beneficial, insufficient, maladaptive, or toxic.

    “Reviews and experimental studies now increasingly describe Alzheimer’s neuroinflammation as a dynamic balance between protective and harmful microglial programs, with disease stage and local tissue environment determining whether immune activation is beneficial, insufficient, maladaptive, or toxic [13,19].”

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Authors
Cai, Y., Liu, J., Wang, B., Sun, M., & Yang, H.
Affiliations
First Affiliated Hospital of Soochow University (CN)
Corresponding author
  • Sun, Miao
  • Yang, Hao
Venue
Frontiers in Immunology
Published
2022-04-26
Volume
13
Pages
856376-856376
ISSN
1664-3224 (ISSN-L)
OpenAlex
W4281554374
Cited by
351
References
169
Citations by year
2026: 70 · 2025: 148 · 2024: 88 · 2023: 41 · 2022: 4
FWCI
7.24
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (81,570,960, 81,974,244, 82071551, 2019YFA0802600)
  • Government of Jiangsu Province
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
microglia, Alzheimer's disease, neuroinflammation, neurodegeneration, amyloid-beta, tau hyperphosphorylation, neurofibrillary tangles, inflammatory cytokines, anti-inflammatory genes, phagocytosis, microglial homeostasis, therapeutic target
MeSH terms
Alzheimer Disease, Humans, Neurons, Amyloid beta-Peptides, Microglia, Neurodegenerative Diseases

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