Evidence map›Paper›PMID 41419972›Full record

ArticleActa neuropathologica communications2025

Vincristine-induced brain toxicity is reduced with prevention of peripheral axon degeneration in Sarm1 knockout mice.

Jonas Yeung, Prisca Hsu, Jordan Mak, Ali Darbandi, Anne L Wheeler, Rosanna Weksberg, Sharon L Guger, Russell J Schachar, Shinya Ito, Johann Hitzler and 1 more

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Jonas YeungMouse Imaging Centre, Hospital for Sick Children, 25 Orde Street, Toronto, ON, M5T 3H7, Canada. jonas.yeung@sickkids.ca.
Prisca HsuNeuroscience and Mental Health, Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Jordan MakNeuroscience and Mental Health, Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Ali DarbandiNanoscale Biomedical Imaging Facility, Hospital for Sick Children, Toronto, ON, Canada.
Anne L WheelerNeuroscience and Mental Health, Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Rosanna WeksbergDepartment of Pediatrics, University of Toronto, Toronto, ON, Canada.
Sharon L GugerDepartment of Psychology, Hospital for Sick Children, Toronto, ON, Canada.
Russell J SchacharInstitutes of Medical Science, University of Toronto, Toronto, ON, Canada.
Shinya ItoTranslational Medicine, Hospital for Sick Children Research Institute, Toronto, ON, Canada.
Johann HitzlerDepartment of Pediatrics, University of Toronto, Toronto, ON, Canada.
Brian J NiemanMouse Imaging Centre, Hospital for Sick Children, 25 Orde Street, Toronto, ON, M5T 3H7, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vincristine is an essential chemotherapy agent administered for various pediatric cancers including acute lymphoblastic leukemia (ALL). While multi-agent chemotherapy for pediatric ALL is highly curative, with survival approaching 95%, it carries the risk of irreversible neurocognitive late effects. Vincristine is known to cause peripheral neuropathy, but its relationship to brain toxicity remains understudied. We investigated vincristine-mediated brain toxicity in young mice lacking Sarm1, a gene whose deletion protects against vincristine-induced peripheral neuropathy. Littermate wildtype and knockout mice were randomly assigned to saline or vincristine groups. In vivo MRI was performed from childhood to early adulthood to measure brain structure volumes, followed by ex vivo diffusion tensor imaging (DTI) to assess microstructural changes. In a separate cohort, electron microscopy (EM) quantified axon morphology in the sciatic nerve and corpus callosum. Vincristine induced significant volume reduction across the brain, while Sarm1 knockout reduced loss in both grey and white matter. Several regions, including the amygdala and dentate gyrus, showed near-complete recovery in knockouts. DTI revealed limited changes with no genotype differences. EM demonstrated vincristine-induced axon morphology alterations in wildtype mice in both the sciatic nerve and corpus callosum. Sarm1 knockout rescued sciatic nerve morphology but not corpus callosum axons. These findings suggest that SARM1-mediated peripheral axon damage may contribute to vincristine-induced brain volume deficits, whereas brain axons may be affected through distinct, SARM1-independent mechanisms. These results suggest a link between vincristine-induced peripheral axon damage and alterations in brain development, with implications for neurocognitive deficits experienced by ALL survivors. Our results suggest that mitigating vincristine-induced peripheral neuropathy may also help reduce neurocognitive deficits in pediatric patients undergoing vincristine treatment.

Indexed as

Antineoplastic Agents, PhytogenicArmadillo Domain ProteinsAxonsBrainCytoskeletal ProteinsNerve DegenerationPeripheral Nervous System DiseasesVincristineAnimalsCorpus CallosumDiffusion Tensor ImagingFemaleMaleMiceMice, Inbred C57BLMice, KnockoutAntineoplastic Agents, PhytogenicArmadillo Domain ProteinsCytoskeletal ProteinsSARM1 protein, mouseVincristineAxon degenerationChemotherapyMRIPeripheral neuropathySARM1Vincristine

Identifiers

PMID41419972
PMCPMC12717744

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.