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Recent advances in molecular pathways and therapeutic implications targeting neuroinflammation for Alzheimer’s disease
Open accessAbstract
Alzheimer's disease (AD) is a major contributor of dementia leading to the degeneration of neurons in the brain with major symptoms like loss of memory and learning. Many evidences suggest the involvement of neuroinflammation in the pathology of AD. Cytokines including TNF-α and IL-6 are also found increasing the BACE1 activity and expression of NFκB resulting in generation of Aβ in AD brain. Following the interaction of Aβ with microglia and astrocytes, other inflammatory molecules also get translocated to the site of inflammation by chemotaxis and exaggerate neuroinflammation. Various pathways like NFκB, p38 MAPK, Akt/mTOR, caspase, nitric oxide and COX trigger microglia to release inflammatory cytokines. PPARγ agonists like pioglitazone increases the phagocytosis of Aβ and reduces inflammatory cytokine IL-1β. Celecoxib and roficoxib like selective COX-2 inhibitors also ameliorate neuroinflammation. Non-selective COX inhibitor indomethacin is also potent inhibitor of inflammatory mediators released from microglia. Mitophagy process is considered quite helpful in reducing inflammation due to microglia as it promotes the phagocytosis of over activated microglial cells and other inflammatory cells. Mitophagy induction is also beneficial in the removal of damaged mitochondria and reduction of infiltration of inflammatory molecules at the site of accumulation of the damaged mitochondria. Targeting these pathways and eventually ameliorating the activation of microglia can mitigate neuroinflammation and come out as a better therapeutic option for the treatment of Alzheimer's disease.
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“Several pathological factors in AD, such as Aβ, pro-inflammatory cytokines, and oxidative stress, activate microglia and initiate downstream signaling pathways such as MAPK, NF-κB, and PI3K/Akt.”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [240]
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“The activation of these pathways further promotes the activation of microglia and the production of inflammatory mediators, exacerbating neurotoxicity.238–240”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [240]
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“A significant trigger for astrocyte reactivity is neuroinflammation, involving pro-inflammatory molecules like cytokines and chemokines (11–14).”
From Varicose projection astrocytes: Conserved reactive cells in brain pathology (2026) · cites this paper as [12]
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“A growing amount of evidence has revealed that a sustained inflammatory state in the brain is a major contributor in the AD pathogenesis (Dhapola et al., 2021).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Dhapola et al., 2021
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“Neuroinflammation has been identified as a key contributor to the pathobiology of AD [2–4]”
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Metadata
- Authors
- Dhapola, R., Hota, S. S., Sarma, P., Bhattacharyya, A., Medhi, B., & Reddy, D. H.
- Affiliations
- Central University of Punjab (IN)
- Post Graduate Institute of Medical Education and Research (IN)
- Government Medical College and Hospital (IN)
- Venue
- Inflammopharmacology
- Published
- 2021-11-23
- Volume
- 29
- Issue
- 6
- Pages
- 1669-1681
- ISSN
- 0925-4692 (ISSN-L)
- 1568-5608
- PMC
- PMC8608577
- OpenAlex
- W3215739089
- Cited by
- 383
- References
- 61
- Citations by year
- 2026: 72 · 2025: 116 · 2024: 111 · 2023: 55 · 2022: 27
- FWCI
- 5.64
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Inflammopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- Alzheimer's disease, neuroinflammation, microglia, amyloid-beta, NF-κB, TNF-α, interleukin-6, p38 MAPK, caspases, nitric oxide, COX-2 inhibitors, PPARγ agonists, pioglitazone, celecoxib, rofecoxib, indomethacin, mitophagy, astrocytes
- MeSH terms
- Neuroinflammatory Diseases, Alzheimer Disease, Animals, Humans, Inflammation, Mitochondria, Cytokines, Inflammation Mediators, Molecular Targeted Therapy, Mitophagy
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