The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets
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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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Experimental — accuracy not yet measuredThe 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].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [50]
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- Authors
- AmeliMojarad, M., & AmeliMojarad, M.
- Affiliations
- National Institute of Genetic Engineering and Biotechnology (IR)
- Corresponding author
- AmeliMojarad, Mandana
- ORCID
- AmeliMojarad, Melika
- Venue
- CNS Neuroscience & Therapeutics
- Publisher
- Wiley
- Published
- 2024-07
- Volume
- 30
- Issue
- 7
- Pages
- e14856-e14856
- ISSN
- 1755-5930 (ISSN-L)
- 1755-5949
- PMC
- PMC11259573
- 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
- gold
- doi.org
- Licence
- 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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