Therapeutic potential of human microglia transplantation in a chimeric model of CSF1R-related leukoencephalopathy
Open accessAbstract
Microglia replacement strategies are increasingly being considered for the treatment of primary microgliopathies like adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP). However, available mouse models fail to recapitulate the diverse neuropathologies and reduced microglia numbers observed in patients. In this study, we generated a xenotolerant mouse model lacking the fms-intronic regulatory element (FIRE) enhancer within Csf1r, which develops nearly all the hallmark pathologies associated with ALSP. Remarkably, transplantation of human induced pluripotent stem cell (iPSC)-derived microglial (iMG) progenitors restores a homeostatic microglial signature and prevents the development of axonal spheroids, white matter abnormalities, reactive astrocytosis, and brain calcifications. Furthermore, transplantation of CRISPR-corrected ALSP-patient-derived iMG reverses pre-existing spheroids, astrogliosis, and calcification pathologies. Together with the accompanying study by Munro and colleagues, our results demonstrate the utility of FIRE mice to model ALSP and provide compelling evidence that iMG transplantation could offer a promising new therapeutic strategy for ALSP and perhaps other microglia-associated neurological disorders.
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Microglial replacement or reprogramming may represent a therapeutic strategy for neurodegenerative and neuroinflammatory disease.
“Several studies have demonstrated that microglial replacement or reprogramming may represent a therapeutic strategy for neurodegenerative and neuroinflammatory disease.”
From Older adult APOE4 mice exhibit modest immunometabolic adaptation following microglial APOE2 replacement (2027) · cites this paper as Chadarevian et al., 2024
The Discussion reports that transplanting healthy or CRISPR-corrected microglia prevented or reversed several pathologies in a mouse model of ALSP. The paper proposes replacement as a possible therapy for ALSP and perhaps other microglia-associated neurological disorders, but the cited passages do not establish therapeutic reprogramming or the broader claim across neurodegenerative and neuroinflammatory diseases. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSHIP1 and SHIP2's enzymatic product, PI(3,4)P2, is found on lysosomal membranes, where it controls lysosome function.
“SHIP1 and SHIP2’s enzymatic product, PI(3,4)P2, is found on lysosomal membranes, where it controls lysosome function66”
From INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia (2025) · cites this paper as [66]
The Results section on axonal spheroids reports lysosome-associated LAMP1 staining, but does not discuss SHIP1, SHIP2, or PI(3,4)P2. Searches for those terms and for phosphatidylinositol 3,4-bisphosphate and lysosome function found no passage addressing the claimed localization or function. (LLM, conf=0.77)
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Glia in Neurodegenerative DiseasePreprint
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- Authors
- Chadarevian, J. P., Hasselmann, J., Lahian, A., Capocchi, J. K., Escobar, A., Lim, T. E., Le, L., Tu, C., Nguyen, J., Kiani Shabestari, S., Carlen-Jones, W., Gandhi, S., Bu, G., Hume, D. A., Pridans, C., Wszolek, Z. K., Spitale, R. C., Davtyan, H., & Blurton-Jones, M.
- Affiliations
- University of California, Irvine (US)
- Hong Kong University of Science and Technology (HK)
- The University of Queensland (AU)
- Centre for Inflammation Research (GB)
- Corresponding author
- Davtyan, Hayk
- Blurton-Jones, Mathew
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2024-08
- Volume
- 112
- Issue
- 16
- Pages
- 2686-2707.e8
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC12357648
- OpenAlex
- W4399775612
- Cited by
- 83
- References
- 101
- Citations by year
- 2026: 32 · 2025: 41 · 2024: 10
- FWCI
- 13.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuron (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, cc-by)
- Rare & Special e-Zone (The Hong Kong University of Science and Technology) (submittedVersion)
- Funders
- Cure Alzheimer's Fund
- National Institutes of Health (1s10od021718-01, 1s10rr025496-01, 1s10od010794-01, T32 AG00096, AG00096, AG066519)
- University of California, Irvine (1S10OD021718-01, 1S10OD010794-01, 1S10RR025496-01)
- National Institute on Aging (AG00096, T32 AG00096, AG066519, AG061895, R01AG061895, U19AG063911, T32AG000096, T32AG073088, U19AG069701, P30AG066519)
- National Cancer Institute (P30CA062203)
- National Institute of Neurological Disorders and Stroke (R43NS124409)
- National Center for Research Resources (S10 RR025496)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- adult-onset leukoencephalopathy with axonal spheroids and pigmented glia, ALSP, CSF1R, axonal swellings, reactive astrogliosis, cerebral calcification, white matter abnormalities
- MeSH terms
- Animals, Disease Models, Animal, Gliosis, Humans, Receptor, Macrophage Colony-Stimulating Factor, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Microglia, Mice, Leukoencephalopathies, Induced Pluripotent Stem Cells
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