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Translational Neurodegeneration

, 6:20

First Online: 11 July 2017Received: 04 January 2017Accepted: 27 June 2017


Traumatic brain injury is among the most common causes of death and disability in youth and young adults. In addition to the acute risk of morbidity with moderate to severe injuries, traumatic brain injury is associated with a number of chronic neurological and neuropsychiatric sequelae including neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. However, despite the high incidence of traumatic brain injuries and the established clinical correlation with neurodegeneration, the causative factors linking these processes have not yet been fully elucidated. Apart from removal from activity, few, if any prophylactic treatments against post-traumatic brain injury neurodegeneration exist. Therefore, it is imperative to understand the pathophysiological mechanisms of traumatic brain injury and neurodegeneration in order to identify potential factors that initiate neurodegenerative processes. Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been implicated in both secondary brain injury and neurodegeneration. In particular, reactive oxygen species appear to be key in mediating molecular insult in neuroinflammation and excitotoxicity. As such, it is likely that post injury oxidative stress is a key mechanism which links traumatic brain injury to increased risk of neurodegeneration. Consequently, reactive oxygen species and their subsequent byproducts may serve as novel fluid markers for identification and monitoring of cellular damage. Furthermore, these reactive species may further serve as a suitable therapeutic target to reduce the risk of post-injury neurodegeneration and provide long term quality of life improvements for those suffering from traumatic brain injury.

KeywordsTraumatic brain injury Neurodegenerative diseases Alzheimer’s disease Parkinson’s disease Amyotrophic lateral sclerosis Oxidative stress Reactive oxygen species AbbreviationsADAlzheimer’s disease

ALSAmyotrophic lateral sclerosis

APPAmyloid precursor protein

AβAmyloid beta

CNSCentral nervous system

CTEChronic traumatic encephalopathy

GLT-1Glutamate transporter 1

mTBIMild traumatic brain injury

PDParkinson’s disease

ROSReactive Oxygen Species

SOD1Superoxide dismutase

TBITraumatic brain injury

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Autor: Marcela Cruz-Haces - Jonathan Tang - Glen Acosta - Joseph Fernandez - Riyi Shi


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