ArticleScientific reports2017
RhoA-ROCK Inhibition Reverses Synaptic Remodeling and Motor and Cognitive Deficits Caused by Traumatic Brain Injury.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Neurodegenerative Disease Associated Pathways in the Brains of Triple Transgenic Alzheimer's Model Mice Are Reversed Following Two Weeks of Peripheral Administration of Fasudil.International journal of molecular sciences · 2023Pooled it
- Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Re-Purposing a Rho-Associated Coiled-Coil Kinase (ROCK) Inhibitor for Alzheimer's Disease.Journal of clinical medicine · 2026Article
- Synaptopathy in cone and rod cells after retinal detachment and reattachment.Experimental eye research · 2026Article
- The Design Strategies and Applications of Engineered Nanoparticles for Traumatic Brain Injury.International journal of nanomedicine · 2026Review
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Sex and Genotype Affect Mouse Hippocampal Gene Expression in Response to Blast-Induced Traumatic Brain Injury.Molecular neurobiology · 2025Article
- Targeting Tiam1 Enhances Hippocampal-Dependent Learning and Memory in the Adult Brain and Promotes NMDA Receptor-Mediated Synaptic Plasticity and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Identification ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The link between impact-induced tensile strain and dendritic spine morphology in porcine brain tissue.PloS one · 2025Article
- From imaging to intervention: emerging potential of PET biomarkers to shape therapeutic strategies for TBI-induced neurodegeneration.Frontiers in neurology · 2025Review
- Viral-mediated increased hippocampal neurogranin modulate synapses at one month in a rat model of controlled cortical impact.Scientific reports · 2024Article
- Article
- The Reduction of Traumatic Spinal Cord Secondary Injury by Anti-RhoA siRNA Functionalized Nucleic Acid Nanoparticles (NANPs).RNA nanomed · 2024Article
- A narrative review of the effects of dexamethasone on traumatic brain injury in clinical and animal studies: focusing on inflammation.Inflammopharmacology · 2023Review
- Neurodevelopmental disorders, like cancer, are connected to impaired chromatin remodelers, PI3K/mTOR, and PAK1-regulated MAPK.Biophysical reviews · 2023Review
- Variable importance for projection (VIP) scores for analyzing the contribution of risk factors in severe adverse events to Xiyanping injection.Chinese medicine · 2023Article
- A photo-switchable assay system for dendrite degeneration and repair inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- TRPV4: A trigger of pathological RhoA activation in neurological disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Therapeutic efficacy of rolipram delivered by PgP nanocarrier on secondary injury and motor function in a rat TBI model.Nanomedicine (London, England) · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) causes extensive neural damage, often resulting in long-term cognitive impairments. Unfortunately, effective treatments for TBI remain elusive. The RhoA-ROCK signaling pathway is a potential therapeutic target since it is activated by TBI and can promote the retraction of dendritic spines/synapses, which are critical for information processing and memory storage. To test this hypothesis, RhoA-ROCK signaling was blocked by RhoA deletion from postnatal neurons or treatment with the ROCK inhibitor fasudil. We found that TBI impairs both motor and cognitive performance and inhibiting RhoA-ROCK signaling alleviates these deficits. Moreover, RhoA-ROCK inhibition prevents TBI-induced spine remodeling and mature spine loss. These data argue that TBI elicits pathological spine remodeling that contributes to behavioral deficits by altering synaptic connections, and RhoA-ROCK inhibition enhances functional recovery by blocking this detrimental effect. As fasudil has been safely used in humans, our results suggest that it could be repurposed to treat TBI.
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