ArticleAge (Dordrecht, Netherlands)2013
Exendin-4 induced glucagon-like peptide-1 receptor activation reverses behavioral impairments of mild traumatic brain injury in mice.
Article in Age (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed.
- Incretin Mimetics as Potential Therapeutics for Concussion and Traumatic Brain Injury: A Narrative Review.International journal of molecular sciences · 2025Review
- Sexually Dimorphic Responses Reveal Multifaceted Benefits of Glibenclamide in Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- The Therapeutic Potential of Glucagon-like Peptide 1 Receptor Agonists in Traumatic Brain Injury.Pharmaceuticals (Basel, Switzerland) · 2024Review
- GLP-1 Receptor Agonists: Beyond Diabetes-What the Neurosurgeon Needs to Know.Neurosurgery practice · 2024Review
- Pharmacological Approaches Using Diabetic Drugs Repurposed for Alzheimer's Disease.Biomedicines · 2024Review
- Metabolic Disorder Therapeutics and their Effects on Memory.CNS & neurological disorders drug targets · 2024Review
- Administration of the GLP-1 receptor agonist exenatide in rats improves functional recovery after spinal cord injury by reducing endoplasmic reticulum stress.IBRO neuroscience reports · 2023Article
- Review
- Glucagon-like peptide-1 (GLP-1) receptor agonists and neuroinflammation: Implications for neurodegenerative disease treatment.Pharmacological research · 2022Review
- Mitigation of Hearing Damage After Repeated Blast Exposures in Animal Model of Chinchilla.Journal of the Association for Research in Otolaryngology : JARO · 2022Article
- Review
- Antidiabetic Drugs in the Treatment of Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Type 2 Diabetes Mellitus as a Risk Factor for Alzheimer's Disease: Review and Meta-Analysis.Biomedicines · 2022Review
- Neuroprotection of Exendin-4 by Enhanced Autophagy in a Parkinsonian Rat Model of α-Synucleinopathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Exendin-4 Preserves Blood-Brain Barrier IntegrityFrontiers in molecular neuroscience · 2021Article
- Astrocytes as Key Regulators of Brain Energy Metabolism: New Therapeutic Perspectives.Frontiers in physiology · 2021Review
- The Effect of Mild Traumatic Brain Injury on Cerebral Microbleeds in Aging.Frontiers in aging neuroscience · 2021Article
- The Neurotrophic Function of Glucagon-Like Peptide-1 Promotes Human Neuroblastoma Differentiation via the PI3K-AKT Axis.Biology · 2020Article
- Motor Effects of Minimal Traumatic Brain Injury in Mice.Journal of molecular neuroscience : MN · 2020Article
- Neurotrophic and neuroprotective effects of a monomeric GLP-1/GIP/Gcg receptor triagonist in cellular and rodent models of mild traumatic brain injury.Experimental neurology · 2020Article
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Authors and funding
9 authors.
Funding
Abstract
Mild traumatic brain injury (mTBI) represents a major and increasing public health concern and is both the most frequent cause of mortality and disability in young adults and a chief cause of morbidity in the elderly. Albeit mTBI patients do not show clear structural brain defects and, generally, do not require hospitalization, they frequently suffer from long-lasting cognitive, behavioral, and emotional problems. No effective pharmaceutical therapy is available, and existing treatment chiefly involves intensive care management after injury. The diffuse neural cell death evident after mTBI is considered mediated by oxidative stress and glutamate-induced excitotoxicity. Prior studies of the long-acting GLP-1 receptor agonist, exendin-4 (Ex-4), an incretin mimetic approved for type 2 diabetes mellitus treatment, demonstrated its neurotrophic/protective activity in cellular and animal models of stroke, Alzheimer's and Parkinson's diseases, and, consequent to commonalities in mechanisms underpinning these disorders, Ex-4 was assessed in a mouse mTBI model. In neuronal cultures in this study, Ex-4 ameliorated H2O2-induced oxidative stress and glutamate toxicity. To evaluate in vivo translation, we administered steady-state Ex-4 (3.5 pM/kg/min) or saline to control and mTBI mice over 7 days starting 48 h prior to or 1 h post-sham or mTBI (30 g weight drop under anesthesia). Ex-4 proved well-tolerated and fully ameliorated mTBI-induced deficits in novel object recognition 7 and 30 days post-trauma. Less mTBI-induced impairment was evident in Y-maze, elevated plus maze, and passive avoidance paradigms, but when impairment was apparent Ex-4 induced amelioration. Together, these results suggest that Ex-4 may act as a neurotrophic/neuroprotective drug to minimize mTBI impairment.
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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.