Traumatic Brain Injury: Role in Induction and Progression of Neurodegenerative Disorders

Author:

Kumar Sumit1,Pooja Pooja2,Kumar Dinesh3,Gulia Sachin4,Rajni Rajni5,Thakur Megha6

Affiliation:

1. Assistant Professor, Department of Pharmaceutical Sciences, Central University of Haryana, Jant-Pali, Mahendergarh, (Haryana), India – 123031.

2. Research Scholar, Department of Pharmaceutical Sciences, Central University of Haryana, Jant-Pali, Mahendergarh, (Haryana), India – 123031.

3. Assistant Professor, Atam Institute of Pharmacy, Om Sterling Global University, Hisar Haryana.

4. School of Pharmacy, Sharda University, Greater Noida, Uttar Pradesh 201306, India.

5. Assistant Professor, Starex University, Gurugram, Haryana.

6. Megha Thakur - School of Pharmacy, Sharda University, Greater Noida, Uttar Pradesh 201306, India.

Abstract

Background: Traumatic brain injury (TBI) affects a huge proportion of population worldwide. TBI is the most common epigenetic health risk for neurological illness later in life. Different post-injury mechanisms may contribute to neurodegeneration. Thus, it is associated with a greater risk of neurodegenerative diseases for instance Parkinson’s disease (PD), depression, epilepsy, amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and chronic traumatic encephalopathy (CTE). Objective: The present study encapsulates the neurodegenerative effects trigged by TBI. Therefore, understanding of such triggers may be helpful in prediction, early diagnosis or the management of neurodegenerative diseases in patients who had TBI. Further, understanding of TBI-induced neuronal damage may provide better knowledge for drug development, disease management, and check of induction and progression of neurodegenerative diseases. Conclusion: Several approaches show a strong correlation between TBI secondary injury and various neurodegenerative diseases involving oxidative stress and numerous neuroinflammationdiseases. It appears that oxidative stress plays a crucial role in both TBI and neurodegeneration by causing neuroinflammation and glutamatergicexcitotoxicity.

Publisher

A and V Publications

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