ArticleNeuroscience and neuroeconomics2017
Neuroprotective effects of estrogen in CNS injuries: insights from animal models.
Article in Neuroscience and neuroeconomics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
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- Neuroprotective Effects of Transcranial Pulsed Current Stimulation: Modulation of Microglial Polarization in Traumatic Brain Injury.CNS neuroscience & therapeutics · 2025Article
- The Influence of Menstrual Cycle Phases on Postconcussion Outcomes and Symptom Reporting: A Scoping Review.Scandinavian journal of medicine & science in sports · 2025Article
- Retina-Targeted 17β-Estradiol by the DHED Prodrug Rescues Visual Function and Actuates Neuroprotective Protein Networks After Optic Nerve Crush in a Rat Model of Surgical Menopause.International journal of molecular sciences · 2025Article
- Gamma-tocotrienol Inhibits Proliferation and Growth of HSD17B4 Overexpressing HepG2 Liver Cancer Cells.Current cancer drug targets · 2025Article
- Ulcerative colitis model triggers gut α-Synuclein aggregation without brain involvement or neuronal loss in female rats.Frontiers in immunology · 2025Article
- CCL5 is essential for axonogenesis and neuronal restoration after brain injury.Journal of biomedical science · 2024Article
- Sex differences in physiological response to increased neuronal excitability in a knockin mouse model of pediatric epilepsy.Clinical science (London, England : 1979) · 2024Article
- TUNEL-n-DIFL Method for Detection and Estimation of Apoptosis Specifically in Neurons and Glial Cells in Mixed Culture and Animal Models of Central Nervous System Diseases and Injuries.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Neuroprotection or Sex Bias: A Protective Response to Traumatic Brain Injury in the Females.CNS & neurological disorders drug targets · 2024Review
- Agomir-331 Suppresses Reactive Gliosis and Neuroinflammation after Traumatic Brain Injury.Cells · 2023Article
- Posttreatment with Ospemifene Attenuates Hypoxia- and Ischemia-Induced Apoptosis in Primary Neuronal Cells via Selective Modulation of Estrogen Receptors.Neurotoxicity research · 2023Article
- Neuroprotective role of Noggin in spinal cord injury.Neural regeneration research · 2023Review
- Dynamic MRI of the Mesenchymal Stem Cells Distribution during Intravenous Transplantation in a Rat Model of Ischemic Stroke.Life (Basel, Switzerland) · 2023Article
- Established and Emerging Therapies in Acute Spinal Cord Injury.Neurospine · 2022Article
- Hyperbaric Oxygen Therapy after Mid-Cervical Spinal Contusion Injury.Journal of neurotrauma · 2022Article
- Dysmetabolism and Neurodegeneration: Trick or Treat?Nutrients · 2022Review
- Premarin Reduces Neurodegeneration and Promotes Improvement of Function in an Animal Model of Spinal Cord Injury.International journal of molecular sciences · 2022Article
- General Anesthesia and the Young Brain: The Importance of Novel Strategies with Alternate Mechanisms of Action.International journal of molecular sciences · 2022Review
- Synthetic neuroactive steroids as new sedatives and anaesthetics: Back to the future.Journal of neuroendocrinology · 2022Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Among the estrogens that are biosynthesized in the human body, 17β-estradiol (estradiol or E2) is the most common and the best estrogen for neuroprotection in animal models of the central nervous system (CNS) injuries such as spinal cord injury (SCI), traumatic brain injury (TBI), and ischemic brain injury (IBI). These CNS injuries are not only serious health problems, but also enormous economic burden on the patients, their families, and the society at large. Studies from animal models of these CNS injuries provide insights into the multiple neuroprotective mechanisms of E2 and also suggest the possibility of translating the therapeutic efficacy of E2 in the treatment SCI, TBI, and IBI in humans in the near future. The pathophysiology of these injuries includes loss of motor function in the limbs, arms and their extremities, cognitive deficit, and many other serious consequences including life-threatening paralysis, infection, and even death. The potential application of E2 therapy to treat the CNS injuries may become a trend as the results are showing significant therapeutic benefits of E2 for neuroprotection when administered into the animal models of SCI, TBI, and IBI. This article describes the plausible mechanisms how E2 works with or without the involvement of estrogen receptors and provides an overview of the known neuroprotective effects of E2 in these three CNS injuries in different animal models. Because activation of estrogen receptors has profound implications in maintaining and also affecting normal physiology, there are notable impediments in translating E2 therapy to the clinics for neuroprotection in CNS injuries in humans. While E2 may not yet be the sole molecule for the treatment of CNS injuries due to the controversies surrounding it, the neuroprotective effects of its metabolite and derivative or combination of E2 with another therapeutic agent are showing significant impacts in animal models that can potentially shape the new treatment strategies for these CNS injuries in humans.
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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.