Decoding the role of the CCL2/CCR2 axis in Alzheimer’s disease and innovating therapeutic approaches: Keeping All options open
Abstract
Alzheimer's disease (AD), as a neurodegenerative disorder, distresses the elderly in large numbers and is characterized by β-amyloid (Aβ) accumulation, elevated tau protein levels, and chronic inflammation. The brain's immune system is aided by microglia and astrocytes, which produce chemokines and cytokines. Nevertheless, dysregulated expression can cause hyperinflammation and lead to neurodegeneration. CCL2/CCR2 chemokines are implicated in neurodegenerative diseases exacerbating. Inflicting damage on nerves and central nervous system (CNS) cells is the function of this axis, which recruits and migrates immune cells, including monocytes and macrophages. It has been shown that targeting the CCL2/CCR2 axis may be a therapeutic option for inflammatory diseases. Using the current knowledge about the involvement of the CCL2/CCR2 axis in the immunopathogenesis of AD, this comprehensive review synthesizes existing information. It also explores potential therapeutic options, including modulation of the CCL2/CCR2 axis as a possible strategy in AD.
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CCL2 has the known capacity to break down the blood brain barrier and recruit peripheral immune cells to sites of damage.
“consistent with the known capacity of CCL2 to break down the blood brain barrier and recruit peripheral immune cells to sites of damage.58–62”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [62]
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- Authors
- Arfaei, R., Mikaeili, N., Daj, F., Boroumand, A., Kheyri, A., Yaraghi, P., Shirzad, Z., Keshavarz, M., Hassanshahi, G., Jafarzadeh, A., Shahrokhi, V. M., & Khorramdelazad, H.
- Affiliations
- Rafsanjan University of Medical Sciences (IR)
- Corresponding author
- Khorramdelazad, Hossein
- Venue
- International Immunopharmacology
- Publisher
- Elsevier BV
- Published
- 2024-06
- Volume
- 135
- Pages
- 112328
- ISSN
- 1567-5769 (ISSN-L)
- OpenAlex
- W4399007042
- Cited by
- 27
- References
- 10
- Citations by year
- 2026: 9 · 2025: 14 · 2024: 4
- FWCI
- 1.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- International Immunopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- Alzheimer's disease, CCL2/CCR2 axis, chemokines, neuroinflammation, microglia, astrocytes, monocyte recruitment, macrophage migration, amyloid-beta, tau protein, immunopathogenesis, therapeutic targeting
- MeSH terms
- Alzheimer Disease, Animals, Brain, Humans, Amyloid beta-Peptides, Chemokine CCL2, Receptors, CCR2
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