Affiliations: 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
Note: [] Corresponding author: Neelima B. Chauhan, Ph.D., R&D (151), Jesse Brown VA Medical Center, 820 South Damen Avenue, Chicago, IL 60612, USA. Tel.: +1 312 569 7747; Fax: +1 312 569 8114; E-mail: nchauhan@uic.edu
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 diseases 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), Apolipoprotein E (ApoE), presenilin (PS) and neprilysin (NEP) genes is associated with exacerbation of neurodegenerative process after TBI. This review encompasses acute effects and chronic neurodegenerative consequences after TBI.
