ArticleScientific reports2017
TrkB-enhancer facilitates functional recovery after 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 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- TrkB promotes the neuronal secretion of soluble Siglec-2 (CD22) to mitigate microglial activation and alleviate depression-like behaviors in male mice.Molecular psychiatry · 2026Article
- The Role of HIF-1α and Its Association with BDNF Levels in Post-Stroke Cognitive Decline Following Prenatal Immune Activation and Maternal Hypoxic Stress in Adult Rat Offspring: A Sex Comparison Study.Molecular neurobiology · 2026Article
- Novel peptidomimetic compounds attenuate hypoxic-ischemic brain injury in neonatal rats.Experimental neurology · 2025Article
- Non-invasive therapeutics for neurotrauma: a mechanistic overview.Frontiers in neurology · 2025Review
- Targeting the postsynaptic scaffolding protein PSD-95 enhances BDNF signaling to mitigate depression-like behaviors in mice.Science signaling · 2024Article
- Structure-based design of peptidomimetic inhibitors of PSD-95 with improved affinity for the PDZ3 domain.FEBS letters · 2024Article
- Neuroprotective Effects of Nanowired Delivery of Cerebrolysin with Mesenchymal Stem Cells and Monoclonal Antibodies to Neuronal Nitric Oxide Synthase in Brain Pathology Following Alzheimer's Disease Exacerbated by Concussive Head Injury.Advances in neurobiology · 2023Review
- Activation of neurotrophin signalling with light‑inducible receptor tyrosine kinases.Molecular medicine reports · 2022Article
- A PDK-1 allosteric agonist neutralizes insulin signaling derangements and beta-amyloid toxicity in neuronal cells and in vitro.PloS one · 2022Article
- Deficits in Acoustic Startle Reactivity and Auditory Temporal Processing after Traumatic Brain Injury.Neurotrauma reports · 2022Article
- An update on the association between traumatic brain injury and Alzheimer's disease: Focus on Tau pathology and synaptic dysfunction.Neuroscience and biobehavioral reviews · 2021Review
- Pathogenic Functions of Tumor Necrosis Factor Receptor-Frontiers in molecular neuroscience · 2021Article
- Vascular and non-vascular contributors to memory reduction during traumatic brain injury.The European journal of neuroscience · 2019Review
- Nicotinamide Improves Functional Recovery via Regulation of the RAGE/JNK/NF-κB Signaling Pathway after Brain Injury.Journal of clinical medicine · 2019Article
- BDNF Val66Met Genetic Polymorphism Results in Poor Recovery Following Repeated Mild Traumatic Brain Injury in a Mouse Model and Treatment With AAV-BDNF Improves Outcomes.Frontiers in neurology · 2019Article
- Hyperbaric Oxygen Alleviates the Inflammatory Response Induced by LPS Through Inhibition of NF-κB/MAPKs-CCL2/CXCL1 Signaling Pathway in Cultured Astrocytes.Inflammation · 2018Article
- Supramolecular Nanostructure Activates TrkB Receptor Signaling of Neuronal Cells by Mimicking Brain-Derived Neurotrophic Factor.Nano letters · 2018Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF), a key player in regulating synaptic strength and learning, is dysregulated following traumatic brain injury (TBI), suggesting that stimulation of BDNF signaling pathways may facilitate functional recovery. This study investigates whether CN2097, a peptidomimetic ligand which targets the synaptic scaffold protein, postsynaptic density protein 95, to enhance downstream signaling of tropomyosin-related kinase B, a receptor for BDNF, can improve neurological function after TBI. Moderate to severe TBI elicits neuroinflammation and c-Jun-N-terminal kinase (JNK) activation, which is associated with memory deficits. Here we demonstrate that CN2097 significantly reduces the post-traumatic synthesis of proinflammatory mediators and inhibits the post-traumatic activation of JNK in a rodent model of TBI. The recordings of field excitatory post-synaptic potentials in the hippocampal CA1 subfield demonstrate that TBI inhibits the expression of long-term potentiation (LTP) evoked by high-frequency stimulation of Schaffer collaterals, and that CN2097 attenuates this LTP impairment. Lastly, we demonstrate that CN2097 significantly improves the complex auditory processing deficits, which are impaired after injury. The multifunctionality of CN2097 strongly suggests that CN2097 could be highly efficacious in targeting complex secondary injury processes resulting from neurotrauma.
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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.