Evidence map›Paper›PMID 42779646›Full record

ArticlebioRxiv : the preprint server for biology2026

Spared corticospinal neurons activate an endogenous plasticity program after partial CNS injury.

Matias Murillo, Ciara F O'Brien, Noa Golan, Emma X Yin, Kristen J Brennand, William B J Cafferty

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. 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

6 authors.

Matias MurilloInterdepartmental Neuroscience Program, Yale University School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0001-6391-8618
Ciara F O'BrienDepartment of Neurology, Yale University School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0002-3139-4298
Noa GolanInterdepartmental Neuroscience Program, Yale University School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0002-1382-9745
Emma X YinDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA.
Kristen J BrennandDepartment of Psychiatry, Yale University School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0003-0993-5956
William B J CaffertyDepartment of Neurology, Yale University School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0001-6263-2167

Funding

High-throughput in vivo and in vitro functional and multi-omics screens of neuropsychiatric and neurodevelopmental disorder risk genesRM1MH132648 · NIMH · YALE UNIVERSITY · PI Kristen Jennifer Brennand, Rong Fan · 2023 to 2026
$5.6M
Modeling the interaction of physiological and environmental stressors on common variants to psychiatric traitsR01ES033630 · NIEHS · YALE UNIVERSITY · PI Kristen Jennifer Brennand · 2022 to 2026
$4.6M
NEUROBIOLOGY OF CORTICAL SYSTEMST32NS007224 · NINDS · YALE UNIVERSITY · PI CARDIN, JESSICA A · 1985 to 2025
$4.6M
Investigating the Effects of Spinal Cord Injury and Rehabilitative Training on Corticospinal Circuits Controlling Contextual Opioid Analgesic ToleranceR01NS121026 · NINDS · YALE UNIVERSITY · PI William B. Cafferty · 2022 to 2026
$2.1M
Team science approach to integrate machine-learning models and functional genomics to study aging in the context of Alzheimer's diseaseR21AG087875 · NIA · YALE UNIVERSITY · PI BRENNAND, KRISTEN JENNIFER, GERSTEIN, MARK BENDER · 2024 to 2025
$459k
Mechanisms that support Raphespinal tract plasticity and regeneration after spinal cord injuryR21NS139481 · NINDS · YALE UNIVERSITY · PI William B. Cafferty · 2025 to 2026
$428k
NIA NIH HHS R21 AG087875NIEHS NIH HHS R01 ES033630NIMH NIH HHS RM1 MH132648NINDS NIH HHS R01 NS121026NINDS NIH HHS R21 NS139481NINDS NIH HHS T32 NS007224
6 · The paper itself

Abstract

Functional recovery after incomplete spinal cord injury depends substantially on the capacity of anatomically spared neurons to remodel their connections, yet the molecular programs underlying this endogenous plasticity remain poorly understood. To identify and validate these mechanisms, we combined retrograde labeling, unilateral corticospinal tract injury, spatial transcriptomics, and human stem cell-derived neurons. Injured corticospinal neurons exhibited widespread downregulation with remaining activated pathways dominated by stress, cell death, and degenerative programs. In contrast, spared corticospinal neurons activated a coordinated pro-plasticity program characterized by metabolic, immune, and cytoskeletal remodeling together with selective suppression of growth-inhibitory signaling. Network and drug perturbation analyses identified

Identifiers

PMID42779646
PMCPMC13596234

What Socratic holds

Textmetadata
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 Socratic graph.