ArticleJournal of neuropathology and experimental neurology2014
Conditional overexpression of insulin-like growth factor-1 enhances hippocampal neurogenesis and restores immature neuron dendritic processes after traumatic brain injury.
Article in Journal of neuropathology and experimental neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
- Adolescent Ethanol Exposure Disrupts the Mature Phenotype of Surviving Neuroprogenitors in Female Mice.Hippocampus · 2026Article
- Reduced inhibition of hippocampal adult-born granule cells by parvalbumin interneurons after TBI.bioRxiv : the preprint server for biology · 2026Article
- CD44 antagonism after traumatic brain injury influences the adult neurogenic niche and behavioral outcomes.Brain structure & function · 2026Article
- Cardioprotection and neurobehavioral impact of swimming training in ovariectomized rats.GeroScience · 2025Article
- Sex-based differences in the long-term fate of hippocampal neurons born after a traumatic brain injury.Frontiers in behavioral neuroscience · 2025Article
- IGF-1's protective effect on OSAS rats' learning and memory.Sleep & breathing = Schlaf & Atmung · 2024Article
- Brain IGF-I regulates LTP, spatial memory, and sexual dimorphic behavior.Life science alliance · 2023Article
- Brain and spinal cord trauma: what we know about the therapeutic potential of insulin growth factor 1 gene therapy.Neural regeneration research · 2023Review
- The role of IGF-1 in exercise to improve obesity-related cognitive dysfunction.Frontiers in neuroscience · 2023Review
- The endogenous progenitor response following traumatic brain injury: a target for cell therapy paradigms.Neural regeneration research · 2022Review
- Insulin-Like Growth Factor-1 Enhances Motoneuron Survival and Inhibits Neuroinflammation After Spinal Cord Transection in Zebrafish.Cellular and molecular neurobiology · 2022Article
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
- Peroxisomal Proliferator-Activated ReceptorFrontiers in pharmacology · 2022Article
- The interplay of neurovasculature and adult hippocampal neurogenesis.Neuroscience letters · 2021Review
- Concussion/Mild Traumatic Brain Injury (TBI) Induces Brain Insulin Resistance: A Positron Emission Tomography (PET) Scanning Study.International journal of molecular sciences · 2021Article
- IGF1-Stimulated Posttraumatic Hippocampal Remodeling Is Not Dependent on mTOR.Frontiers in cell and developmental biology · 2021Article
- Dendritic arbor complexity and spine density changes after repetitive mild traumatic brain injury and neuroprotective treatments.Brain research · 2020Article
- Oligodendrocyte Response to Pathophysiological Conditions Triggered by Episode of Perinatal Hypoxia-Ischemia: Role of IGF-1 Secretion by Glial Cells.Molecular neurobiology · 2020Article
- A Western diet impairs CNS energy homeostasis and recovery after spinal cord injury: Link to astrocyte metabolism.Neurobiology of disease · 2020Article
- Neuroinflammatory Gene Expression Alterations in Anterior Cingulate Cortical White and Gray Matter of Males With Autism Spectrum Disorder.Autism research : official journal of the International Society for Autism Research · 2020Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is associated with neuronal damage or neuronal death in the hippocampus, a region critical for cognitive function. Immature neurons within the hippocampal neurogenic niche are particularly susceptible to TBI. Therapeutic strategies that protect immature hippocampal neurons or enhance posttraumatic neurogenesis may be advantageous for promoting functional recovery after TBI. Insulin-like growth factor-1 (IGF-1) promotes neurogenesis in the adult brain, but its effects on neurogenesis after TBI are unknown. We used an astrocyte-specific conditional IGF-1-overexpressing mouse model to supplement IGF-1 in regions of neuronal damage and reactive astrocytosis after controlled cortical impact injury. Although early loss of immature neurons was not significantly attenuated, overexpression of IGF-1 resulted in a marked increase in immature neuron density in the subgranular zone at 10 days after injury. This delayed increase seemed to be driven by enhanced neuron differentiation rather than by increased cellular proliferation. In wild-type mice, dendrites of immature neurons exhibited significant decreases in total length and number of bifurcations at 10 days after injury versus neurons in sham-injured mice. In contrast, the morphology of immature neuron dendrites in brain-injured IGF-1-overexpressing mice was equivalent to that in sham controls. These data provide compelling evidence that IGF-1 promotes neurogenesis after TBI.
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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.