Title:Traumatic Brain Injury as a Risk Factor for Alzheimer’s Disease: Is Inflammatory Signaling a Key Player?
VOLUME: 13 ISSUE: 7
Author(s):Jelena Djordjevic, Mohammad Golam Sabbir and Benedict C. Albensi
Affiliation:Division of Neurodegenerative Disorders, St. Boniface Hospital Research Winnipeg, Manitoba, Canada.
Keywords:Alzheimer's disease, inflammation, mitochondria, NF-κB, Traumatic brain injury.
Abstract: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.
