Citation

Corrigan F, Arulsamy A, Teng J, Collins-Praino L. J. Neurotrauma 2016; 34(5): 971-986.

Affiliation

University of Adelaide, School of Medicine , Frome Rd , Adelaide, South Australia, Australia , 5005 ; lyndsey.collins-praino@adelaide.edu.au.

Copyright

(Copyright © 2016, Mary Ann Liebert Publishers)

DOI

10.1089/neu.2016.4589

PMID

27630018

Abstract

Traumatic brain injury (TBI) is the leading cause of disability and death worldwide, affecting as many as 54-60 million people annually. TBI is associated with significant impairments in brain function, impacting cognitive, emotional, behavioral and physical functioning. While much previous research has focused on the impairment immediately following injury, TBI may have much longer-lasting consequences, including neuropsychiatric disorders and cognitive impairment. TBI, even mild head injury, has also been recognized as a significant risk factor for the later development of dementia and Alzheimer's disease. While the link between TBI and dementia is currently unknown, several proposed mechanisms have been put forward, including alterations in glucose metabolism, excitotoxicity, calcium influx, mitochondrial dysfunction, oxidative stress and neuroinflammation. A treatment for the devastating long-term consequences of TBI is desperately needed. Unfortunately, however, no such treatment is available, making this a major area of unmet medical need. Increasing the level of neurotrophic factor expression in key brain areas may be one potential therapeutic strategy. Of the neurotrophic factors, granulocyte-colony stimulating factor (G-CSF) may be particularly effective for preventing the emergence of long-term complications of TBI, including dementia, due to its ability to reduce apoptosis, stimulate neurogenesis and increase neuroplasticity.

Language: en