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Journal Article

Citation

Griesbach GS, Masel BE, Helvie RE, Ashley M. J. Neurotrauma 2018; 35(1): 17-24.

Affiliation

Centre for Neuro Skills, Bakersfield, California, United States ; mashley@neuroskills.com.

Copyright

(Copyright © 2018, Mary Ann Liebert Publishers)

DOI

unavailable

PMID

28920532

Abstract

The acute and chronic effects of traumatic brain injury (TBI) have been widely described; however, there is limited knowledge on how a TBI sustained during early or mid adulthood will influence aging. Epidemiological studies have explored whether TBI poses a risk for dementia and other neurodegenerative diseases associated with aging. We will discuss the influence of TBI and resulting medical comorbidities such as endocrine, sleep and inflammatory disturbances on age-related grey and white matter changes and cognitive decline.. Post-mortem studies examining amyloid, tau and other proteins will be discussed within the context of neurodegenerative diseases and chronic traumatic encephalopathy. The data support the suggestion that pathological changes triggered by an earlier TBI will have an influence on normal aging processes and will interact with neurodegenerative disease processes, rather than the development of a specific disease, such as Alzheimer's or Parkinson's. Chronic neurophysiologic change after TBI may have detrimental effects on neurodegenerative disease.


Language: en

Keywords

BETA AMYLOID; NEURODEGENERATIVE DISORDERS; TRAUMATIC BRAIN INJURY

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