Cited by 74Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsNeurological Disease Mechanisms and Treatments

The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets

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AmeliMojarad, Melika, AmeliMojarad, Mandana·2024·CNS Neuroscience & Therapeutics

Abstract

Introduction: Alzheimer's disease (AD), the main cause of dementia, is characterized by synaptic loss and neurodegeneration. Amyloid‐β (Aβ) accumulation, hyperphosphorylation of tau protein, and neurofibrillary tangles (NFTs) in the brain are considered to be the initiating factors of AD. However, this hypothesis falls short of explaining many aspects of AD pathogenesis. Recently, there has been mounting evidence that neuroinflammation plays a key role in the pathophysiology of AD and causes neurodegeneration by over‐activating microglia and releasing inflammatory mediators. Methods: PubMed, Web of Science, EMBASE, and MEDLINE were used for searching and summarizing all the recent publications related to inflammation and its association with Alzheimer's disease. Results: Our review shows how inflammatory dysregulation influences AD pathology as well as the roles of microglia in neuroinflammation, the possible microglia‐associated therapeutic targets, top neuroinflammatory biomarkers, and anti‐inflammatory drugs that combat inflammation. Conclusion: In conclusion, microglial inflammatory reactions are important factors in AD pathogenesis and need to be discussed in more detail for promising therapeutic strategies.

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  • Microglia can compact plaques, clear amyloid-β, remove debris, regulate lipid stress, support repair, and coordinate local tissue responses, even while they can also produce cytokines, engage complement-mediated synapse loss, and contribute to chronic inflammatory injury.

    “Microglia can compact plaques, clear amyloid-β, remove debris, regulate lipid stress, support repair, and coordinate local tissue responses, even while they can also produce cytokines, engage complement-mediated synapse loss, and contribute to chronic inflammatory injury.”

    From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [50]

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  • The challenge is not simply to reduce inflammation, but to modulate it with enough precision to preserve protective microglial activity while preventing maladaptive activation.

    “Recent reviews of neuroinflammation therefore emphasize that the challenge is not simply to reduce inflammation, but to modulate it with enough precision to preserve protective microglial activity while preventing maladaptive activation [50,51].”

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Research works printed but not linked: 2

  1. [94]Zheng C, Zhou XW, Wang JZ. The dual roles of cytokines in Alzheimer's disease: update on interleukins, TNF‐α, TGF‐β and IFN‐γ. Transl Neurodegener. 2016; 5: 7. 27054030 PMC4822284
  2. [116]Kanazawa M, Kawamura K, Takahashi T, Nishizawa M, Shimohata T. Progranulin. Nihon Rinsho. 2016; 74: 579‐ 582. 27333743

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Authors
AmeliMojarad, M., & AmeliMojarad, M.
Affiliations
National Institute of Genetic Engineering and Biotechnology (IR)
Corresponding author
AmeliMojarad, Mandana
Venue
CNS Neuroscience & Therapeutics
Publisher
Wiley
Published
2024-07
Volume
30
Issue
7
Pages
e14856-e14856
ISSN
  • 1755-5930 (ISSN-L)
  • 1755-5949
OpenAlex
W4400856584
Cited by
73
References
155
Citations by year
2026: 38 · 2025: 32 · 2024: 3
FWCI
3.72
Type
journal article
Language
en
Open access
Locations
  • CNS Neuroscience & Therapeutics (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
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
Alzheimer's disease, microglia, neuroinflammation, amyloid-beta, tau hyperphosphorylation, neurofibrillary tangles, neurodegeneration, neuroinflammatory biomarkers, anti-inflammatory agents, therapeutic target
MeSH terms
Neuroinflammatory Diseases, Alzheimer Disease, Animals, Anti-Inflammatory Agents, Humans, Inflammation, Microglia

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