Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy
Open accessAbstract
Though motor neurons selectively degenerate in amyotrophic lateral sclerosis, other cell types are likely involved in this disease. We recently generated rNLS8 mice in which human TDP-43 (hTDP-43) pathology could be reversibly induced in neurons and expected that microglia would contribute to neurodegeneration. However, only subtle microglial changes were detected during disease in the spinal cord, despite progressive motor neuron loss; microglia still reacted to inflammatory triggers in these mice. Notably, after hTDP-43 expression was suppressed, microglia dramatically proliferated and changed their morphology and gene expression profiles. These abundant, reactive microglia selectively cleared neuronal hTDP-43. Finally, when microgliosis was blocked during the early recovery phase using PLX3397, a CSF1R and c-kit inhibitor, rNLS8 mice failed to regain full motor function, revealing an important neuroprotective role for microglia. Therefore, reactive microglia exert neuroprotective functions in this amyotrophic lateral sclerosis model, and definition of the underlying mechanism could point toward novel therapeutic strategies.
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The existence of DAM in mice and humans has recently been confirmed in tauopathy AD models, aging, and other neurodegenerative diseases such as ALS and multiple sclerosis.
“The existence of DAM in mice and humans has recently been confirmed in tauopathy AD models (26, 27), aging (27, 28), and other neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) (29) and multiple sclerosis (30).”
From Therapeutic Idol reduction ameliorates amyloidosis and improves cognitive function in APP/PS1 mice (2020) · cites this paper as [29]
The Results section on transcriptomic profiling (page unavailable) reports that genes previously called DAM were upregulated in microglia from an ALS-relevant mouse model during both late disease and early recovery. This supports the ALS mouse-model portion of the citation, but the paper does not establish a DAM population in humans: its human ALS analysis assesses reactive microgliosis, not DAM identity. The other diseases in the citing sentence have separate citations and are not assessed here. (LLM, conf=0.87)
Experimental — accuracy not yet measuredMicroglia actively facilitate clearance of hTDP-43 in a transgenic TDP-43 mouse model.
“There is also evidence that microglia actively facilitate the clearance of hTDP-43 in a transgenic TDP-43 mouse model.342”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [342]
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- Authors
- Spiller, K. J., Restrepo, C. R., Khan, T., Dominique, M. A., Fang, T. C., Canter, R. G., Roberts, C. J., Miller, K. R., Ransohoff, R. M., Trojanowski, J. Q., & Lee, V. M.-Y.
- Affiliations
- University of Pennsylvania (US)
- Biogen (United States) (US)
- Corresponding author
- Spiller, Krista J.
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2018-02-20
- Volume
- 21
- Issue
- 3
- Pages
- 329-340
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC5857237
- OpenAlex
- W2788797941
- Cited by
- 301
- References
- 50
- Citations by year
- 2026: 17 · 2025: 31 · 2024: 48 · 2023: 32 · 2022: 33 · 2021: 47 · 2020: 37 · 2019: 36 · 2018: 20
- FWCI
- 24.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- ALS Association
- Judith and Jean Pape Adams Charitable Foundation
- Biogen
- National Institute on Aging (P30AG010124, P01AG017586, T32AG000255)
- National Institute of Neurological Disorders and Stroke (R01NS110688)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Keywords
- amyotrophic lateral sclerosis, TDP-43 proteinopathy, microglia, microglial activation, motor neuron degeneration, neuroprotection, PLX3397, CSF1R inhibition, c-kit inhibition, motor recovery, spinal cord
- MeSH terms
- Superoxide Dismutase-1, Aminopyridines, Amyotrophic Lateral Sclerosis, Animals, Gliosis, Humans, Inflammation, Mice, Transgenic, Motor Neurons, Mutation, Pyrroles, Spinal Cord, Muscle, Skeletal, Recovery of Function, Gene Expression Profiling, Myeloid Cells, Mice, TDP-43 Proteinopathies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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