ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2012
Genetic manipulation of cell death and neuroplasticity pathways in traumatic brain injury.
Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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.
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.
Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Amyloid-beta peptide toxicity in the aged brain is a one-way journey into Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Withania somnifera inhibits photorefractoriness which triggers neuronal apoptosis in both pre-optic and paraventricular hypothalamic area of Coturnix coturnix japonica: involvement of oxidative stress induced p53 dependent Caspase-3 mediated low immunoreactivity of estrogen receptor alpha.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2023Article
- Autophagy machinery plays an essential role in traumatic brain injury-induced apoptosis and its related behavioral abnormalities in mice: focus onFrontiers in physiology · 2023Article
- Compensatory cognition in neurological diseases and aging: A review of animal and human studies.Aging brain · 2023Review
- Review
- The Roles of Neurotrophins in Traumatic Brain Injury.Life (Basel, Switzerland) · 2021Review
- Altered Topological Properties of Grey Matter Structural Covariance Networks in Complete Thoracic Spinal Cord Injury Patients: A Graph Theoretical Network Analysis.Neural plasticity · 2021Article
- Mechanosensation in traumatic brain injury.Neurobiology of disease · 2021Review
- A Moderate Blast Exposure Results in Dysregulated Gene Network Activity Related to Cell Death, Survival, Structure, and Metabolism.Frontiers in neurology · 2020Article
- Role of Pyroptosis in Traumatic Brain and Spinal Cord Injuries.International journal of biological sciences · 2020Review
- Review
- Incretin Mimetics as Rational Candidates for the Treatment of Traumatic Brain Injury.ACS pharmacology & translational science · 2019Article
- Antioxidant activity and apoptotic induction as mechanisms of action of Withania somnifera (Ashwagandha) against a hepatocellular carcinoma cell line.The Journal of international medical research · 2018Article
- Repeated Neonatal Sevoflurane Exposure-Induced Developmental Delays of Parvalbumin Interneurons and Cognitive Impairments Are Reversed by Environmental Enrichment.Molecular neurobiology · 2017Article
- Understanding the Mechanisms of Recovery and/or Compensation following Injury.Neural plasticity · 2017Review
- Function and Mechanisms of Autophagy in Brain and Spinal Cord Trauma.Antioxidants & redox signaling · 2015Review
- Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric comorbidities.Molecular neurobiology · 2014Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) initiates a complex cascade of secondary neurodegenerative mechanisms contributing to cell dysfunction and necrotic and apoptotic cell death. The injured brain responds by activating endogenous reparative processes to counter the neurodegeneration or remodel the brain to enhance functional recovery. A vast array of genetically altered mice provide a unique opportunity to target single genes or proteins to better understand their role in cell death and endogenous repair after TBI. Among the earliest targets for transgenic and knockout studies in TBI have been programmed cell death mediators, such as the Bcl-2 family of proteins, caspases, and caspase-independent pathways. In addition, the role of cell cycle regulatory elements in the posttraumatic cell death pathway has been explored in mouse models. As interest grows in neuroplasticity in TBI, the use of transgenic and knockout mice in studies focused on gliogenesis, neurogenesis, and the balance of growth-promoting and growth-inhibiting molecules has increased in recent years. With proper consideration of potential effects of constitutive gene alteration, traditional transgenic and knockout models can provide valuable insights into TBI pathobiology. Through increasing sophistication of conditional and cell-type specific genetic manipulations, TBI studies in genetically altered mice will be increasingly useful for identification and validation of novel therapeutic targets.
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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.