The DOI matches its Crossref record; 168 of the 169 references it cites were found in a registry or an index.
Microglia in the Neuroinflammatory Pathogenesis of Alzheimer’s Disease and Related Therapeutic Targets
Open accessAbstract
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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“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 central unresolved issue is that the same broad category of “microglial activation” can describe processes with opposite biological consequences.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [19]
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“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].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [19]
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Metadata
- 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
- Publisher
- Frontiers Media SA
- Published
- 2022-04-26
- Volume
- 13
- Pages
- 856376-856376
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC9086828
- 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
- gold
- doi.org
- Licence
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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