ArticleFrontiers in molecular neuroscience2022
SARM1 Depletion Slows Axon Degeneration in a CNS Model of Neurotropic Viral Infection.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections.Journal of neuroinflammation · 2025Article
- Gap junction intercellular communications regulates activation of SARM1 and protects against axonal degeneration.Cell death & disease · 2025Article
- SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- NMNAT2 is a druggable target to drive neuronal NAD production.Nature communications · 2024Article
- Programmed axon death: a promising target for treating retinal and optic nerve disorders.Eye (London, England) · 2024Review
- Abnormal Intraepidermal Nerve Fiber Density in Disease: A Scoping Review.medRxiv : the preprint server for health sciences · 2023Article
- SARM1 detection in myelinating glia:Frontiers in cellular neuroscience · 2023Article
- Abnormal intraepidermal nerve fiber density in disease: A scoping review.Frontiers in neurology · 2023Article
- Axon Biology in ALS: Mechanisms of Axon Degeneration and Prospects for Therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Zika virus (ZIKV) is a neurotropic flavivirus recently linked to congenital ZIKV syndrome in children and encephalitis and Guillain-Barré syndrome in adults. Neurotropic viruses often use axons to traffic to neuronal or glial cell somas where they either remain latent or replicate and proceed to infect new cells. Consequently, it has been suggested that axon degeneration could represent an evolutionarily conserved mechanism to limit viral spread. Whilst it is not known if ZIKV transits in axons, we previously reported that ZIKV infection of glial cells in a murine spinal cord-derived cell culture model of the CNS is associated with a profound loss of neuronal cell processes. This, despite that postmitotic neurons are relatively refractory to infection and death. Here, we tested the hypothesis that ZIKV-associated degeneration of neuronal processes is dependent on activation of Sterile alpha and armadillo motif-containing protein 1 (SARM1), an NADase that acts as a central executioner in a conserved axon degeneration pathway. To test this, we infected wild type and
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.