TY - JOUR
T1 - Aging with a traumatic brain injury
T2 - Could behavioral morbidities and endocrine symptoms be influenced by microglial priming?
AU - Ziebell, Jenna M.
AU - Rowe, Rachel K.
AU - Muccigrosso, Megan M.
AU - Reddaway, Jack T.
AU - Adelson, P. David
AU - Godbout, Jonathan P.
AU - Lifshitz, Jonathan
N1 - Funding Information:
Efforts to prepare this manuscript were partially supported by Mission Support Funds from Barrow Neurological Institute at Phoenix Children’s Hospital and the Bruce and Diane Halle Foundation . Additional support was provided by an NIA grant ( R01-AG-033028 to J.P.G.), a College of Medicine Dean’s Discovery Grant (to J.P.G.), funding from the Center for Brain and Spinal Cord Repair (to J.P.G.). R.K.R. was supported by a Bisgrove Fellowship from Science Foundation Arizona .
Funding Information:
Efforts to prepare this manuscript were partially supported by Mission Support Funds from Barrow Neurological Institute at Phoenix Children's Hospital and the Bruce and Diane Halle Foundation. Additional support was provided by an NIA grant (R01-AG-033028 to J.P.G.), a College of Medicine Dean's Discovery Grant (to J.P.G.), funding from the Center for Brain and Spinal Cord Repair (to J.P.G.). R.K.R. was supported by a Bisgrove Fellowship from Science Foundation Arizona.
Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2017/1/1
Y1 - 2017/1/1
N2 - A myriad of factors influence the developmental and aging process and impact health and life span. Mounting evidence indicates that brain injury, even moderate injury, can lead to lifetime of physical and mental health symptoms. Therefore, the purpose of this mini-review is to discuss how recovery from traumatic brain injury (TBI) depends on age-at-injury and how aging with a TBI affects long-term recovery. TBI initiates pathophysiological processes that dismantle circuits in the brain. In response, reparative and restorative processes reorganize circuits to overcome the injury-induced damage. The extent of circuit dismantling and subsequent reorganization depends as much on the initial injury parameters as other contributing factors, such as genetics and age. Age-at-injury influences the way the brain is able to repair itself, as a result of developmental status, extent of cellular senescence, and injury-induced inflammation. Moreover, endocrine dysfunction can occur with TBI. Depending on the age of the individual at the time of injury, endocrine dysfunction may disrupt growth, puberty, influence social behaviors, and possibly alter the inflammatory response. In turn, activation of microglia, the brain's immune cells, after injury may continue to fuel endocrine dysfunction. With age, the immune system develops and microglia become primed to subsequent challenges. Sustained inflammation and microglial activation can continue for weeks to months post-injury. This prolonged inflammation can influence developmental processes, behavioral performance and age-related decline. Overall, brain injury may influence the aging process and expedite glial and neuronal alterations that impact mental health.
AB - A myriad of factors influence the developmental and aging process and impact health and life span. Mounting evidence indicates that brain injury, even moderate injury, can lead to lifetime of physical and mental health symptoms. Therefore, the purpose of this mini-review is to discuss how recovery from traumatic brain injury (TBI) depends on age-at-injury and how aging with a TBI affects long-term recovery. TBI initiates pathophysiological processes that dismantle circuits in the brain. In response, reparative and restorative processes reorganize circuits to overcome the injury-induced damage. The extent of circuit dismantling and subsequent reorganization depends as much on the initial injury parameters as other contributing factors, such as genetics and age. Age-at-injury influences the way the brain is able to repair itself, as a result of developmental status, extent of cellular senescence, and injury-induced inflammation. Moreover, endocrine dysfunction can occur with TBI. Depending on the age of the individual at the time of injury, endocrine dysfunction may disrupt growth, puberty, influence social behaviors, and possibly alter the inflammatory response. In turn, activation of microglia, the brain's immune cells, after injury may continue to fuel endocrine dysfunction. With age, the immune system develops and microglia become primed to subsequent challenges. Sustained inflammation and microglial activation can continue for weeks to months post-injury. This prolonged inflammation can influence developmental processes, behavioral performance and age-related decline. Overall, brain injury may influence the aging process and expedite glial and neuronal alterations that impact mental health.
KW - Aging
KW - Cognition
KW - Endocrine dysfunction
KW - Inflammation
KW - Microglia
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=84961773396&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84961773396&partnerID=8YFLogxK
U2 - 10.1016/j.bbi.2016.03.008
DO - 10.1016/j.bbi.2016.03.008
M3 - Review article
C2 - 26975888
AN - SCOPUS:84961773396
SN - 0889-1591
VL - 59
SP - 1
EP - 7
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -