Inhibition of NADPH oxidase 2 (NOX2) reverses cognitive deficits by modulating excitability and excitatory transmission in the hippocampus after traumatic brain injury
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry,Biophysics
Reference21 articles.
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2. Changing patterns in the epidemiology of traumatic brain injury;Roozenbeek;Nat. Rev. Neurol.,2013
3. Translating the oxidative stress hypothesis into the clinic: NOX versus NOS;Armitage;J. Mol. Med. (Berl.),2009
4. The role of NOX inhibitors in neurodegenerative diseases;Barua;IBRO Rep.,2019
5. NOX2 complex-derived ROS as immune regulators;Sareila;Antioxidants Redox Signal.,2011
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1. Traumatic brain injury: Mechanisms, manifestations, and visual sequelae;Frontiers in Neuroscience;2023-02-23
2. Gamma frequency entrainment rescues cognitive impairment by decreasing postsynaptic transmission after traumatic brain injury;CNS Neuroscience & Therapeutics;2023-02-05
3. Effects of NADPH Oxidase Isoform-2 (NOX2) Inhibition on Behavioral Responses and Neuroinflammation in a Mouse Model of Neuropathic Pain;Biomedicines;2023-01-31
4. Synaptic and mitochondrial alterations in traumatic brain injury (TBI): neuroprotective effects of phytochemicals and herbal products;Ayurvedic Herbal Preparations in Neurological Disorders;2023
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