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Traumatic Brain Injury as a Risk Factor for Alzheimer’s Disease: Is Inflammatory Signaling a Key Player?

[ Vol. 13 , Issue. 7 ]


Jelena Djordjevic, Mohammad Golam Sabbir and Benedict C. Albensi   Pages 730 - 738 ( 9 )


Traumatic brain injury (TBI) has become a significant medical and social concern within the last 30 years. TBI has acute devastating effects, and in many cases, seems to initiate long-term neurodegeneration. With advances in medical technology, many people are now surviving severe brain injuries and their long term consequences. Post trauma effects include communication problems, sensory deficits, emotional and behavioral problems, physical complications and pain, increased suicide risk, dementia, and an increased risk for chronic CNS diseases, such as Alzheimer’s disease (AD).

In this review, we provide an introduction to TBI and hypothesize how it may lead to neurodegenerative disease in general and AD in particular. In addition, we discuss the evidence that supports the hypothesis that TBI may lead to AD. In particular, we focus on inflammatory responses as key processes in TBI-induced secondary injury, with emphasis on nuclear factor kappa B (NF-κB) signaling.


Alzheimer's disease, inflammation, mitochondria, NF-κB, Traumatic brain injury.


Division of Neurodegenerative Disorders, St. Boniface Hospital Research Winnipeg, Manitoba, Canada.

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