Chronic neurodegenerative consequences of traumatic brain injury

Restor Neurol Neurosci. 2014;32(2):337-65. doi: 10.3233/RNN-130354.

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.

Keywords: Alzheimer's disease; Parkinson's disease; Traumatic brain injury; amyotrophic lateral sclerosis; chronic traumatic encephalopathy; dementia; dementia pugilistica; traumatic axonal injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Amyloid beta-Protein Precursor / metabolism*
  • Animals
  • Brain Injuries / complications
  • Brain Injuries / metabolism*
  • Chronic Disease
  • Humans
  • Neurodegenerative Diseases / complications
  • Neurodegenerative Diseases / metabolism*
  • Neurons / cytology
  • Neurons / metabolism*
  • Risk Factors

Substances

  • Amyloid beta-Protein Precursor