ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2013
Scriptaid, a novel histone deacetylase inhibitor, protects against traumatic brain injury via modulation of PTEN and AKT pathway : scriptaid protects against TBI via AKT.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Systematic review and meta-analysis of experimental studies evaluating the organ protective effects of histone deacetylase inhibitors.Translational research : the journal of laboratory and clinical medicine · 2019Pooled it
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- Age-Dependent Changes in Taurine, Serine, and Methionine Release in the Frontal Cortex of Awake Freely-Moving Rats: A Microdialysis Study.Life (Basel, Switzerland) · 2025Article
- Reversing Persistent PTEN Activation after Traumatic Brain Injury Fuels Long-Term Axonal Regeneration via Akt/mTORC1 Signaling Cascade.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RNA Interference Unleashed: Current Perspective of Small Interfering RNA (siRNA) Therapeutics in the Treatment of Neuropathic Pain.ACS pharmacology & translational science · 2024Review
- CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway.Journal of neuroinflammation · 2024Article
- Microglial histone deacetylase 2 is dispensable for functional and histological outcomes in a mouse model of traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Activation of Beta-adrenergic Receptors Upregulates the Signal-to-Noise Ratio of Auditory Input in the Medial Prefrontal Cortex and Mediates Auditory Fear Conditioning.Molecular neurobiology · 2024Article
- Emerging Neuroprotective Strategies: Unraveling the Potential of HDAC Inhibitors in Traumatic Brain Injury Management.Current neuropharmacology · 2024Review
- Bystanders or not? Microglia and lymphocytes in aging and stroke.Neural regeneration research · 2023Review
- Netrin-3 Suppresses Diabetic Neuropathic Pain by Gating the Intra-epidermal Sprouting of Sensory Axons.Neuroscience bulletin · 2023Article
- Overexpressed ski efficiently promotes neurorestoration, increases neuronal regeneration, and reduces astrogliosis after traumatic brain injury.Gene therapy · 2023Article
- Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases.Frontiers in neuroscience · 2023Article
- Review
- Microglia-specific deletion of histone deacetylase 3 promotes inflammation resolution, white matter integrity, and functional recovery in a mouse model of traumatic brain injury.Journal of neuroinflammation · 2022Article
- Essential role of MALAT1 in reducing traumatic brain injury.Neural regeneration research · 2022Article
- Effect of Hypothermia Therapy on Children with Traumatic Brain Injury: A Meta-Analysis of Randomized Controlled Trials.Brain sciences · 2022Review
- Spatial and temporal dynamics of HDACs class IIa following mild traumatic brain injury in adult rats.Molecular psychiatry · 2022Article
- Carbonyl Reductase 1 Attenuates Ischemic Brain Injury by Reducing Oxidative Stress and Neuroinflammation.Translational stroke research · 2021Article
- Oncolytic Viruses in Combination Therapeutic Approaches with Epigenetic Modulators: Past, Present, and Future Perspectives.Cancers · 2021Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Traumatic brain injury (TBI) is a leading cause of motor and cognitive deficits in young adults for which there is no effective therapy. The present study characterizes the protective effect of a new histone deacetylase inhibitor, Scriptaid (Sigma-Aldrich Corporation, St. Louis, MO), against injury from controlled cortical impact (CCI). Scriptaid elicited a dose-dependent decrease in lesion size at 1.5 to 5.5 mg/kg and a concomitant attenuation in motor and cognitive deficits when delivered 30 minutes postinjury in a model of moderate TBI. Comparable protection was achieved even when treatment was delayed to 12 h postinjury. Furthermore, the protection of motor and cognitive functions was long lasting, as similar improvements were detected 35 days postinjury. The efficacy of Scriptaid (Sigma-Aldrich Corporation) was manifested as an increase in surviving neurons, as well as the number/length of their processes within the CA3 region of the hippocampus and the pericontusional cortex. Consistent with other histone deacetylase inhibitors, Scriptaid treatment prevented the decrease in phospho-AKT (p-AKT) and phosphorylated phosphatase and tensin homolog deleted on chromosome 10 (p-PTEN) induced by TBI in cortical and CA3 hippocampal neurons. Notably, the p-AKT inhibitor LY294002 attenuated the impact of Scriptaid, providing mechanistic evidence that Scriptaid functions partly by modulating the prosurvival AKT signaling pathway. As Scriptaid offers long-lasting neuronal and behavioral protection, even when delivered 12 h after controlled cortical impact, it is an excellent new candidate for the effective clinical treatment of TBI.
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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.