Roles of Microglial and Monocyte Chemokines and Their Receptors in Regulating Alzheimer's Disease-Associated Amyloid-β and Tau Pathologies
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Chemokines and their receptors have been shown to affect amyloid-β (Aβ) and tau pathologies in mouse models of Alzheimer's disease (AD) by regulating microglia and monocyte-associated neuroinflammation, microglial movement and monocyte recruitment into the brain. These cells in turn can promote and mediate Aβ phagocytosis and degradation and tau phosphorylation. In this review we discuss published work in this field in mouse models of AD and review what is known about the contributions of microglial and monocyte chemokines and their receptors to amyloid and tau pathologies. We focus on the roles of the chemokine/chemokine receptor pairs CCL2/CCR2, CX3CL1/CX3CR1, CCL5/CCR5, CXCL10/CXCR3 and CXCL1/CXCR2, highlighting important knowledge gaps in this field. A full understanding of the functions of chemokines and their receptors in AD may guide the development of novel immunotherapies for this devastating disease.
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Chemokines regulate migration of immune cells to the site of inflammation in neurodegenerative diseases, including AD.
“Chemokines regulate migration of immune cells (e.g., monocytes and microglia) to the site of inflammation in neurodegenerative diseases, including AD (31).”
From Deletion of <i>Abi3</i> gene locus exacerbates neuropathological features of Alzheimer’s disease in a mouse model of Aβ amyloidosis (2021) · cites this paper as [31]
Complete deletion of CX3CR1 is associated with worsening memory deficits and tau pathology.
“However, such complete deletion has also been associated with worsening memory deficits and tau pathology (28–31).”
From Heterozygous CX3CR1 Deficiency in Microglia Restores Neuronal β-Amyloid Clearance Pathways and Slows Progression of Alzheimer's Like-Disease in PS1-APP Mice (2019) · cites this paper as [30]
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Preparation of Primary Mixed Glial Cell Cultures from Adult Mouse Spinal Cord Tissue
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- Authors
- Guedes, J. R., Lao, T., Cardoso, A. L., & El Khoury, J.
- Affiliations
- Harvard University (US)
- Centro de Neurociências e Biologia Celular (PT)
- Venue
- Frontiers in Neurology
- Publisher
- Frontiers Media SA
- Published
- 2018-08-14
- Volume
- 9
- Pages
- 549-549
- ISSN
- 1664-2295 (ISSN-L)
- PMC
- PMC6104478
- OpenAlex
- W2808735182
- Cited by
- 115
- References
- 88
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 12 · 2023: 29 · 2022: 14 · 2021: 12 · 2020: 17 · 2019: 12 · 2018: 2
- FWCI
- 1.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Frontiers in Neurology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (RF1 AG051506, R01 AI119065)
- 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, chemokines, chemokine receptors, microglia, monocytes, amyloid-beta, tau pathology, neuroinflammation, microglial migration, monocyte recruitment, amyloid-beta phagocytosis, tau phosphorylation, CCL2/CCR2, CX3CL1/CX3CR1, immunotherapy
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