2019•International Journal of Health & Allied SciencesRequires access

A review article: Brain damage and neuroplastic responses

Debela Tolessa Yadate, AdugnaChala Wari, Kelil Haji Bedane, GizawMamo Gebayehu

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Abstract

Globally, brain damage is becoming a major problem which can be caused by trauma, cerebrovascular disorders, brain tumors, and infectious diseases. Traumatic brain injury and cerebrovascular disorders are considered highly prevalent and given attention in this review. Their pathology is almost identical and includes oxidative damage, excitotoxicity, and several inflammatory events that lead to neurological damage and finally to death. Both traumatic brain damage and stroke induce hypoxia and glucose deprivation in brain tissue which lead to excessive accumulation of calcium and sodium ions within brain cells and release of glutamate into the extracellular compartment. All of these progress to the production of reactive oxygen species leading to oxidative damage, excitotoxicity, and inflammatory damage which can also activate cell death signaling molecules and finally to neural death. Brain regeneration (neuroplasticity) is potential future therapies in the treatment of brain damage. Neuroplasticity is the capacity of the nervous system to restore brain structure and functions. This could be due to the regrowth of axons whose peripheral projections were damaged, restoration of damaged nerve cells and production of new nerve cells which replace the lost one. This issue is especially important because most of the current drugs are not effective or are limited to symptomatic management. Oxidative damage inhibitors, glutamate inhibitors, anti-inflammatory inhibitors, anti-cell death signaling molecules, and agents promoting neural cell regeneration are among the current targeted strategies for the treatment of brain damage. Therefore, this review summarized the major cause of brain injury and mechanisms involved in the process of neuroplastic response.

About this research paper

What this paper is about

Globally, brain damage is becoming a major problem which can be caused by trauma, cerebrovascular disorders, brain tumors, and infectious diseases. Traumatic brain injury and cerebrovascular disorders are considered highly prevalent and given attention in this review. Their pathology is almost identical and includes oxidative damage, excitotoxicity, and several inflammatory events that lead to neurological damage and finally to death. Both traumatic brain damage and stroke induce hypoxia and glucose deprivation in brain tissue which lead to excessive accumulation of calcium and sodium ions within brain cells and release of glutamate into the extracellular compartment. All of these progress to the production of reactive oxygen species leading to oxidative damage, excitotoxicity, and inflammatory damage which can also activate cell death signaling molecules and finally to neural death. Brain regeneration (neuroplasticity) is potential future therapies in the treatment of brain damage. Neuroplasticity is the capacity of the nervous system to restore brain structure and functions. This could be due to the regrowth of axons whose peripheral projections were damaged, restoration of damaged nerve cells and production of new nerve cells which replace the lost one. This issue is especially important because most of the current drugs are not effective or are limited to symptomatic management. Oxidative damage inhibitors, glutamate inhibitors, anti-inflammatory inhibitors, anti-cell death signaling molecules, and agents promoting neural cell regeneration are among the current targeted strategies for the treatment of brain damage. Therefore, this review summarized the major cause of brain injury and mechanisms involved in the process of neuroplastic response.

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Available abstract

Globally, brain damage is becoming a major problem which can be caused by trauma, cerebrovascular disorders, brain tumors, and infectious diseases. Traumatic brain injury and cerebrovascular disorders are considered highly prevalent and given attention in this review. Their pathology is almost identical and includes oxidative damage, excitotoxicity, and several inflammatory events that lead to neurological damage and finally to death. Both traumatic brain damage and stroke induce hypoxia and glucose deprivation in brain tissue which lead to excessive accumulation of calcium and sodium ions within brain cells and release of glutamate into the extracellular compartment. All of these progress to the production of reactive oxygen species leading to oxidative damage, excitotoxicity, and inflammatory damage which can also activate cell death signaling molecules and finally to neural death. Brain regeneration (neuroplasticity) is potential future therapies in the treatment of brain damage. Neuroplasticity is the capacity of the nervous system to restore brain structure and functions. This could be due to the regrowth of axons whose peripheral projections were damaged, restoration of damaged nerve cells and production of new nerve cells which replace the lost one. This issue is especially important because most of the current drugs are not effective or are limited to symptomatic management. Oxidative damage inhibitors, glutamate inhibitors, anti-inflammatory inhibitors, anti-cell death signaling molecules, and agents promoting neural cell regeneration are among the current targeted strategies for the treatment of brain damage. Therefore, this review summarized the major cause of brain injury and mechanisms involved in the process of neuroplastic response.

Key concepts: Excitotoxicity, Brain damage, Glutamate receptor, Neuroscience, Neuroplasticity, Neuroprotection, Medicine, Programmed cell death

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