Citation

Chauhan NB. Restor. Neurol. Neurosci. 2014; 32(2): 337-365.

Affiliation

Neuroscience Research, Jesse Brown VA Medical Center, Chicago, IL, USA Department of Pediatrics, University of Illinois at Chicago, IL, USA Children's Hospital of the University of Illinois, Chicago, IL, USA.

Copyright

(Copyright © 2014, IOS Press)

DOI

10.3233/RNN-130354

PMID

24398724

Abstract

Traumatic brain injury (TBI) is a serious public health concern and a major cause of death and disability worldwide. Each year, an estimated 1.7 million Americans sustain TBI of which ~52,000 people die, ~275,000 people are hospitalized and 1,365,000 people are treated as emergency outpatients. Currently there are ~5.3 million Americans living with TBI. TBI is more of a disease process than of an event that is associated with immediate and long-term sensomotor, psychological and cognitive impairments. TBI is the best known established epigenetic risk factor for later development of neurodegenerative conditions and dementia. People sustaining TBI are ~4 times more likely to develop dementia at a later stage than people without TBI. Single brain injury is linked to later development of symptoms resembling Alzheimer's disease while repetitive brain injuries are linked to later development of chronic traumatic encephalopathy (CTE) and/or Dementia Pugilistica (DP). Furthermore, genetic background of ß-amyloid precursor protein (APP), ApolipoproteinE (ApoE), presenilin (PS) and neprilysin (NEP) genes is associated with exacerbation of neurodegenerative process after TBI. This review encompasses acute and chronic effects after TBI with a particular emphasis on chronic neurodegenerative consequences of TBI.

Language: en