Rising Stars: Astrocytes as a Therapeutic Target for ALS Disease
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is a multifactorial disease, characterized by a progressive loss of motor neurons that eventually leads to paralysis and death. The current ALS-approved drugs modestly change the clinical course of the disease. The mechanism by which motor neurons progressively degenerate remains unclear but entails a non-cell autonomous process. Astrocytes impaired biological functionality were implicated in multiple neurodegenerative diseases, including ALS, frontotemporal dementia (FTD), Parkinson's disease (PD), and Alzheimer disease (AD). In ALS disease patients, A1 reactive astrocytes were found to play a key role in the pathology of ALS disease and death of motor neurons, via loss or gain of function or acquired toxicity. The contribution of astrocytes to the maintenance of motor neurons by diverse mechanisms makes them a promising therapeutic candidate for the treatment of ALS. Therapeutic approaches targeting at modulating the function of endogenous astrocytes or replacing lost functionality by transplantation of healthy astrocytes, may contribute to the development of therapies which might slow down or even halt the progression ALS diseases. The proposed mechanisms by which astrocytes can potentially ameliorate ALS progression and the status of ALS clinical studies involving astrocytes are discussed.
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Progression of TDP-43 proteinopathies involves non-cell-autonomous signaling among multiple cell types, including astrocytes, microglia, and neurons.
“Progression of TDP-43 proteinopathies involves non-cell-autonomous signaling among multiple cell types, including astrocytes, microglia, and neurons (Clarke & Patani 2020, Izrael et al. 2020, Vahsen et al. 2021).”
From The Role of Retrotransposons and Endogenous Retroviruses in Age-Dependent Neurodegenerative Disorders (2024) · cites this paper as Izrael et al. 2020
In “Role and Therapeutic Potential of Astrocytes in ALS” (page unavailable), the review reports TDP-43 pathology spreading between motor neurons and astrocytes and describes astrocyte-mediated effects on neurons. “Other Strategies Targeting Astrocytes Activity” (page unavailable) discusses astrocyte–microglia signaling in ALS, but does not link that signaling specifically to progression of TDP-43 proteinopathies. The claim combines these findings more broadly than the source supports. (LLM, conf=0.86)
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Self-citationGotkine, M., Caraco, Y., Lerner, Y., Blotnick, S., Wanounou, M., Slutsky, S. G., Chebath, J., Kuperstein, G., Estrin, E., Ben-Hur, T., et al. (2023) · Figshare · doi:10.6084/m9.figshare.22616732
Self-citationLiu, H. (2021) · theses.fr (ABES) · doi:10.70675/5a9f2da3zbf5bz475czba47zc4c2a7f9d903
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- Authors
- Izrael, M., Slutsky, S. G., & Revel, M.
- Affiliations
- Weizmann Institute of Science (IL)
- Corresponding author
- Izrael, Michal
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-07-28
- Volume
- 14
- Pages
- 824-824
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC7399224
- OpenAlex
- W3046035119
- Cited by
- 73
- References
- 114
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 11 · 2023: 14 · 2022: 17 · 2021: 14 · 2020: 1
- FWCI
- 1.29
- Type
- journal article
- Language
- de
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- amyotrophic lateral sclerosis, astrocytes, motor neuron degeneration, non-cell autonomous neurodegeneration, astrocyte transplantation, astrocyte-targeted therapy, neurodegenerative diseases
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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