ArticleInvestigative ophthalmology & visual science2014
Early detection of subclinical visual damage after blast-mediated TBI enables prevention of chronic visual deficit by treatment with P7C3-S243.
Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- P7C3 Compounds as Targeted Mitochondrial Therapeutics for Brain Disorders.CNS neuroscience & therapeutics · 2026Pooled it
- P7C3-A20 prevents whole brain radiotherapy-induced chronic hippocampal redox imbalance and neuropsychiatric impairment in mice.Redox biology · 2026Article
- Pharmacologic reversal of advanced Alzheimer's disease in mice and identification of potential therapeutic nodes in human brain.Cell reports. Medicine · 2026Article
- Impact of blast exposure on visual pathway: Mechanism exploration and novel diagnostic perspectives.PloS one · 2026Article
- Repetitive hypoxic preconditioning protects retinal ganglion cells against damage caused by exposure to blast.PloS one · 2026Article
- Eyes Are the Windows to the Soul: Reviewing the Possible Use of the Retina to Indicate Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Clinical Applications of the Cone Contrast Test in Ophthalmology and Neurology.Journal of clinical medicine · 2025Review
- Dysregulation of Retinal Melatonin Biosynthetic Pathway and Differential Expression of Retina-Specific Genes Following Blast-Induced Ocular Injury in Ferrets.Neurology international · 2025Article
- Alzheimer's Disease and Vascular Dementia, Connecting and Differentiating Features.Current Alzheimer research · 2025Review
- Acutely blocking excessive mitochondrial fission prevents chronic neurodegeneration after traumatic brain injury.Cell reports. Medicine · 2024Article
- Henle fiber layer thickening and deficits in objective retinal function in participants with a history of multiple traumatic brain injuries.Frontiers in neurology · 2024Article
- Higher concentration of P7C3 than required for neuroprotection suppresses renal cell carcinoma growth and metastasis.Journal of Cancer · 2024Article
- Application of P7C3 Compounds to Investigating and Treating Acute and Chronic Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- LongitudinalCell reports methods · 2023Article
- Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.Biomedicines · 2023Review
- Current and future therapeutic strategies for Alzheimer's disease: an overview of drug development bottlenecks.Frontiers in aging neuroscience · 2023Review
- Impairments of retinal hemodynamics and oxygen metrics in ocular hypertension-induced ischemia-reperfusion.Experimental eye research · 2022Article
- Biological Correlations and Confounders for Quantification of Retinal Ganglion Cells by Optical Coherence Tomography Based on Studies of Outbred Mice.Translational vision science & technology · 2022Article
- Neuro-Visual and Vestibular Manifestations of Concussion and Mild TBI.Current neurology and neuroscience reports · 2022Review
- Mesenchymal stem cell secretome protects against oxidative stress-induced ocular blast visual pathologies.Experimental eye research · 2022Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
purposeTraumatic brain injury (TBI) frequently leads to chronic visual dysfunction. The purpose of this study was to investigate the effect of TBI on retinal ganglion cells (RGCs), and to test whether treatment with the novel neuroprotective compound P7C3-S243 could prevent in vivo functional deficits in the visual system.
methodsBlast-mediated TBI was modeled using an enclosed over-pressure blast chamber. The RGC physiology was evaluated using a multielectrode array and pattern electroretinogram (PERG). Histological analysis of RGC dendritic field and cell number were evaluated at the end of the study. Visual outcome measures also were evaluated based on treatment of mice with P7C3-S243 or vehicle control.
resultsWe show that deficits in neutral position PERG after blast-mediated TBI occur in a temporally bimodal fashion, with temporary recovery 4 weeks after injury followed by chronically persistent dysfunction 12 weeks later. This later time point is associated with development of dendritic abnormalities and irreversible death of RGCs. We also demonstrate that ongoing pathologic processes during the temporary recovery latent period (including abnormalities of RGC physiology) lead to future dysfunction of the visual system. We report that modification of PERG to provocative postural tilt testing elicits changes in PERG measurements that correlate with a key in vitro measures of damage: the spontaneous and light-evoked activity of RGCs. Treatment with P7C3-S243 immediately after injury and throughout the temporary recovery latent period protects mice from developing chronic visual system dysfunction.
conclusionsProvocative PERG testing serves as a noninvasive test in the living organism to identify early damage to the visual system, which may reflect corresponding damage in the brain that is not otherwise detectable by noninvasive means. This provides the basis for developing an earlier diagnostic test to identify patients at risk for developing chronic CNS and visual system damage after TBI at an earlier stage when treatments may be more effective in preventing these sequelae. In addition, treatment with the neuroprotective agent P7C3-S243 after TBI protects from visual system dysfunction after TBI.
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