ORCID Profile
0000-0002-4398-6493
Current Organisations
U.S. Department of Veterans Affairs
,
University of Arizona
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Publisher: MyJove Corporation
Date: 12-05-2015
DOI: 10.3791/52293
Publisher: Elsevier BV
Date: 09-2017
Publisher: Springer Science and Business Media LLC
Date: 15-04-2014
Publisher: Elsevier BV
Date: 11-2014
DOI: 10.1016/J.EXPNEUROL.2014.06.008
Abstract: Juvenile traumatic brain injury (TBI) leaves survivors facing a potential lifetime of cognitive, somatic and emotional symptoms. A recent study published in Experimental Neurology (K er et al., 2013) explored the chronic consequences of focal brain injury induced in the juvenile animal, extending their previous observations out to 6months post-injury. The results demonstrate transient, persistent, and late onset behavioral dysfunction, which are associated with subtle evidence for enduring histopathology. In line with investigations about chronic traumatic encephalopathy from brain injury initiated in the adult, juvenile TBI establishes signs of a chronic brain disorder, with unique considerations relative to ongoing developmental processes. This commentary discusses the challenges in evaluating aging with injury in the juvenile population, the current methods of juvenile TBI, and what can be anticipated for the future of the field.
Publisher: Informa UK Limited
Date: 08-12-2015
Publisher: Elsevier BV
Date: 2017
DOI: 10.1016/J.BBI.2016.03.008
Abstract: 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 in idual 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.
Publisher: Elsevier BV
Date: 12-2012
Location: United States of America
Location: United States of America
No related grants have been discovered for Jonathan Lifshitz.