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      Traumatic brain injury: Mechanisms, manifestations, and visual sequelae

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          Abstract

          Traumatic brain injury (TBI) results when external physical forces impact the head with sufficient intensity to cause damage to the brain. TBI can be mild, moderate, or severe and may have long-term consequences including visual difficulties, cognitive deficits, headache, pain, sleep disturbances, and post-traumatic epilepsy. Disruption of the normal functioning of the brain leads to a cascade of effects with molecular and anatomical changes, persistent neuronal hyperexcitation, neuroinflammation, and neuronal loss. Destructive processes that occur at the cellular and molecular level lead to inflammation, oxidative stress, calcium dysregulation, and apoptosis. Vascular damage, ischemia and loss of blood brain barrier integrity contribute to destruction of brain tissue. This review focuses on the cellular damage incited during TBI and the frequently life-altering lasting effects of this destruction on vision, cognition, balance, and sleep. The wide range of visual complaints associated with TBI are addressed and repair processes where there is potential for intervention and neuronal preservation are highlighted.

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          Most cited references330

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          Neurotoxic reactive astrocytes are induced by activated microglia

          A reactive astrocyte subtype termed A1 is induced after injury or disease of the central nervous system and subsequently promotes the death of neurons and oligodendrocytes.
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            The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

            For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.
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              Oxidative Stress and Antioxidant Defense

              Abstract Reactive oxygen species (ROS) are produced by living organisms as a result of normal cellular metabolism and environmental factors, such as air pollutants or cigarette smoke. ROS are highly reactive molecules and can damage cell structures such as carbohydrates, nucleic acids, lipids, and proteins and alter their functions. The shift in the balance between oxidants and antioxidants in favor of oxidants is termed “oxidative stress.” Regulation of reducing and oxidizing (redox) state is critical for cell viability, activation, proliferation, and organ function. Aerobic organisms have integrated antioxidant systems, which include enzymatic and nonenzymatic antioxidants that are usually effective in blocking harmful effects of ROS. However, in pathological conditions, the antioxidant systems can be overwhelmed. Oxidative stress contributes to many pathological conditions and diseases, including cancer, neurological disorders, atherosclerosis, hypertension, ischemia/perfusion, diabetes, acute respiratory distress syndrome, idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. In this review, we summarize the cellular oxidant and antioxidant systems and discuss the cellular effects and mechanisms of the oxidative stress.
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                Author and article information

                Contributors
                Journal
                Front Neurosci
                Front Neurosci
                Front. Neurosci.
                Frontiers in Neuroscience
                Frontiers Media S.A.
                1662-4548
                1662-453X
                23 February 2023
                2023
                : 17
                : 1090672
                Affiliations
                [1] 1The Fresno Institute of Neuroscience , Fresno, CA, United States
                [2] 2NYU Long Island School of Medicine , Mineola, NY, United States
                [3] 3Department of Neuroscience, University of California, Santa Barbara , Santa Barbara, CA, United States
                [4] 4NYU Grossman School of Medicine , New York, NY, United States
                Author notes

                Edited by: Allen Ming Yan Cheong, The Hong Kong Polytechnic University, Hong Kong SAR, China

                Reviewed by: Eric Lowell Singman, Johns Hopkins Medicine, United States; Ronald Schuchard, Envision, Inc., United States

                *Correspondence: Allison B. Reiss, allison.reiss@ 123456NYULangone.org

                This article was submitted to Visual Neuroscience, a section of the journal Frontiers in Neuroscience

                Article
                10.3389/fnins.2023.1090672
                9995859
                36908792
                e4fd6ecd-5e56-4341-81d5-f7325cc1d06e
                Copyright © 2023 Rauchman, Zubair, Jacob, Rauchman, Pinkhasov, Placantonakis and Reiss.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 05 November 2022
                : 06 February 2023
                Page count
                Figures: 2, Tables: 0, Equations: 0, References: 330, Pages: 18, Words: 18827
                Categories
                Neuroscience
                Review

                Neurosciences
                traumatic brain injury,light sensitivity,contrast sensitivity,neuroinflammation,visual acuity,headache,oxidative stress

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