Molecular Mechanisms of Microglial Motility: Changes in Ageing and Alzheimer’s Disease
Open accessAbstract
Microglia are the tissue-resident immune cells of the central nervous system, where they constitute the first line of defense against any pathogens or injury. Microglia are highly motile cells and in order to carry out their function, they constantly undergo changes in their morphology to adapt to their environment. The microglial motility and morphological versatility are the result of a complex molecular machinery, mainly composed of mechanisms of organization of the actin cytoskeleton, coupled with a “sensory” system of membrane receptors that allow the cells to perceive changes in their microenvironment and modulate their responses. Evidence points to microglia as accountable for some of the changes observed in the brain during ageing, and microglia have a role in the development of neurodegenerative diseases, such as Alzheimer’s disease. The present review describes in detail the main mechanisms driving microglial motility in physiological conditions, namely, the cytoskeletal actin dynamics, with emphasis in proteins highly expressed in microglia, and the role of chemotactic membrane proteins, such as the fractalkine and purinergic receptors. The review further delves into the changes occurring to the involved proteins and pathways specifically during ageing and in Alzheimer’s disease, analyzing how these changes might participate in the development of this disease.
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CAP1 plays a role in facilitating the release of CFL1 from ADP-actin filaments.
“CAP1 plays a role in facilitating the release of CFL1 from ADP-actin filaments [29].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [29]
Section 3 (page unavailable) links CAP1 to CFL1 up-regulation during actin remodeling, supporting a role for CAP1 in CFL1 regulation. It does not say that CAP1 facilitates CFL1 release from ADP-actin filaments; searches for that mechanism found no such passage. (LLM, conf=0.78)
Experimental — accuracy not yet measuredThe ACTR2 (encoding ARP2) and CFL1 (Cofilin 1) genes play significant roles in actin remodeling, enabling both baseline movement (ruffling or branching) and chemotactic motility (migration).
“The ACTR2 (encoding ARP2) and CFL1 (Cofilin 1) genes play significant roles in actin remodeling, enabling both baseline movement (ruffling or branching) and chemotactic motility (migration) [18, 28, 29].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [29]
Cytoskeleton reorganization is necessary to carry out these processes.
“At the molecular level, cytoskeleton reorganization is necessary to carry out these processes [29].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [29]
ARP2, CAP1, and CFL1 are proteins related to engulfment processes through actin-based motility mechanisms, and were recently associated with AD resilience according to protein coexpression analysis.
“In this context, ARP2, CAP1, and CFL1 are proteins related to engulfment processes through actin-based motility mechanisms [28, 29], that were recently associated with AD resilience according to protein coexpression analysis [39].”
From Enhanced microglial dynamics and a paucity of tau seeding in the amyloid plaque microenvironment contribute to cognitive resilience in Alzheimer’s disease (2024) · cites this paper as [29]
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“The ACTR2 (encoding ARP2) and CFL1 (Cofilin 1) genes play significant roles in actin remodeling, enabling both baseline movement (ruf-fling or branching) and chemotactic motility (migration) [18, 28, 29].”
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- Authors
- Franco-Bocanegra, D. K., McAuley, C., Nicoll, J. A. R., & Boche, D.
- Affiliations
- University of Southampton (GB)
- University Hospital Southampton NHS Foundation Trust (GB)
- Corresponding author
- Boche, Delphine
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2019-06-25
- Volume
- 8
- Issue
- 6
- Pages
- 639
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC6627151
- OpenAlex
- W2955533479
- Cited by
- 147
- References
- 123
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 20 · 2023: 21 · 2022: 20 · 2021: 28 · 2020: 22 · 2019: 3
- FWCI
- 1.90
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Consejo Nacional de Ciencia y Tecnología (270152/438262)
- University of Southampton (VCFoM/BocheD/TBC/170)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- microglial motility, microglial morphology, actin cytoskeleton dynamics, fractalkine, purinergic receptors, chemotaxis, aging, Alzheimer's disease, neuroinflammation
- MeSH terms
- Aging, Alzheimer Disease, Cell Movement, Humans, Actin Cytoskeleton, Receptors, Purinergic, Microglia
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