Abi3 regulates microglial ramification and dynamic tissue surveillance in vivo
Open accessAbstract
A rare coding variant of Abelson-interactor gene family member 3 (Abi3) is associated with increased risk of late-onset Alzheimer’s Disease (AD). Although Abi3 is recognised as a core microglial gene, its role in microglia is largely unknown. Here we demonstrate that Abi3 is crucial for normal microglial morphology, distribution, and homeostatic tissue surveillance activity in vivo .
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Abi3-Gngt2−/− microglia exhibit reduced surveillance of brain parenchyma.
“Indeed, a recent study suggests that Abi3-Gngt2−/− microglia exhibits reduced surveillance of brain parenchyma [46].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [46]
The paper reports reduced surveillance of brain parenchyma by Abi3-KO microglia in awake mice (Abstract; page unavailable). It does not establish this finding for the Abi3-Gngt2−/− genotype named in the citing sentence; its methods describe Abi3-KO mice crossed with a Cx3cr1-EGFP reporter line (Two-photon microscopy; page unavailable). (LLM, conf=0.88)
Experimental — accuracy not yet measuredAbsence of Abi3 alters microglial morphology and curbs homeostatic surveillance.
“Another recent paper showed that absence of Abi3 (using the same models as used in this study) alters microglial morphology and curbs its function in homeostatic surveillance [46, 47].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [46]
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Cites
Complement and microglia mediate early synapse loss in Alzheimer mouse models
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Cited by
Sorted by citations
The effect of Abi3 locus deletion on the progression of Alzheimer’s disease-related pathologies
Karahan, H., Smith, D. C., Kim, B., McCord, B., Mantor, J., John, S. K., Al-Amin, M. M., Dabin, L. C., & Kim, J. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1102530 · Cited by 20 · see citing works
“Another study reported an increase in the number of IBA1-positive cells, although the total area covered by IBA1 staining was decreased in Abi3 mice without amyloid pathology (47).”
BackgroundDeletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways
Ibanez, K. R., McFarland, K. N., Phillips, J., Allen, M., Lessard, C. B., Zobel, L., De La Cruz, E. G., Shah, S., Vo, Q., Wang, X., et al. (2022) · Alzheimer's Research & Therapy · doi:10.1186/s13195-022-01044-1 · Cited by 18 · see citing works
Scott-Solache, J., Pei, J., Drew, J., López-Doménech, G., Jolivet, R. B., Nieto-Rostro, M., Davenport, E. C., Arancibia-Cárcamo, I. L., Attwell, D., & Kittler, J. T. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2532488123 · Cited by 2 · see citing works
“Genetic deletion of Abi3 , another member of the WRC, also increases CD68 volume in microglia (71).”
- Authors
- Simonazzi, E., Jones, R. E., Chen, F., Ranson, A., Stevenson-Hoare, J., Escott-Price, V., Sengpiel, F., Morgan, B. P., & Taylor, P. R.
- Affiliations
- UK Dementia Research Institute (GB)
- Cardiff University (GB)
- Universitat Autònoma de Barcelona (ES)
- Corresponding author
- Taylor, Philip R.
- Venue
- bioRxiv (Cold Spring Harbor Laboratory)
- Publisher
- openRxiv
- Published
- 2021-03-19
- OpenAlex
- W3137332272
- Cited by
- 3
- References
- 4
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 1
- Type
- posted content
- Language
- en
- Open access
- green
- doi.org
- Licence
- Locations
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- Funders
- Wellcome Trust (107964/Z/15/Z, /Z/15/Z)
- UK Dementia Research Institute
- Medical Research Council (MR/P024939/1)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- ABI3, microglia, microglial ramification, microglial morphology, microglial homeostasis, late-onset Alzheimer's disease, genetic risk variants
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