TBI for Dummies, the research pt 2

Traumatic brain injury, neuroimaging, and neurodegeneration. 2013
Bigler ED
"The first phase of neural degeneration is explainable by the primary acute and secondary neuropathological effects initiated by the injury; however, neuroimaging studies demonstrate a prolonged period of pathological changes that progressively occur even during the chronic phase."
Departments of Exercise and Sport Science, University of North Carolina at Chapel Hill, 27599, USA
http://www.ncbi.nlm.nih.gov/pubmed/23964217

Chronic neuropathological and neurobehavioral changes in a repetitive mTBI model. 2013
Mouzon BC, Bachmeier C, Ferro A, Ojo JO, Crynen G, Acker CM, Davies P, Mullan M, Stewart W, Crawford F.
"Importantly, these data provide evidence that, whilst a single mTBI produces a clinical syndrome and pathology which remain static in the period following injury, repetitive injuries produce behavioral and pathological changes which continue to evolve many months after the initial injuries."
Roskamp Institute, Sarasota, Florida, 34243, USA; James A. Haley Veterans Administration Medical Center, Tampa, Florida, 33612, USA; The Open University, Department of Life Sciences, Milton Keynes, MK, 7 6AA, UK
http://www.ncbi.nlm.nih.gov/pubmed/24243523

New perspectives on central and peripheral immune responses to acute traumatic brain injury. 2012
Das M, Mohapatra S, Mohapatra SS.
"TBI of any form can cause cognitive, behavioral and immunologic changes in later life, which underscores the problem of underdiagnosis of mild TBI that can cause long-term neurological deficits."
Nanomedicine Research Center, University of South Florida Morsani College of Medicine, 12901 Bruce B. Downs Blvd., Tampa, FL 33612, USA.
http://www.ncbi.nlm.nih.gov/pubmed/23061919

Traumatic brain injury: a risk factor for Alzheimer's disease. 2012
Sivanandam TM, Thakur MK.
"Traumatic brain injury (TBI) constitutes a major global health and socio-economic problem with neurobehavioral sequelae contributing to long-term disability. It causes brain swelling, axonal injury and hypoxia, disrupts blood brain barrier function and increases inflammatory responses, oxidative stress, neurodegeneration and leads to cognitive impairment."
Biochemistry and Molecular Biology Laboratory, Department of Zoology, Banaras Hindu University, Varanasi 221005, India.
http://www.ncbi.nlm.nih.gov/pubmed/22390915

Axonal pathology in traumatic brain injury. 2013
Johnson VE, Stewart W, Smith DH.
"Diffuse axonal injury (DAI) has been found in all severities of TBI and may represent a key pathologic substrate of mild TBI (concussion). [...] In addition, recent evidence suggests that TBI may induce long-term neurodegenerative processes, such as insidiously progressive axonal pathology. Indeed, axonal degeneration has been found to continue even years after injury in humans, and appears to play a role in the development of Alzheimer's disease-like pathological changes."
Penn Center for Brain Injury and Repair and Department of Neurosurgery, University of Pennsylvania, PA 19104, USA.
http://www.ncbi.nlm.nih.gov/pubmed/22285252

Traumatic brain injury: an overview of pathobiology with emphasis on military populations. 2010
Cernak I, Noble-Haeusslein LJ.
"This review considers the pathobiology of non-impact blast-induced neurotrauma (BINT). The pathobiology of traumatic brain injury (TBI) has been historically studied in experimental models mimicking features seen in the civilian population. These brain injuries are characterized by primary damage to both gray and white matter and subsequent evolution of secondary pathogenic events at the cellular, biochemical, and molecular levels, which collectively mediate widespread neurodegeneration."
National Security Technology Department, Johns Hopkins University Applied Physics Laboratory, Laurel, Maryland 20723, USA
http://www.ncbi.nlm.nih.gov/pubmed/19809467

Whole-brain proton MR spectroscopic imaging of mild-to-moderate traumatic brain injury and correlation with neuropsychological deficits. 2010
Govind V, Gold S, Kaliannan K, Saigal G, Falcone S, Arheart KL, Harris L, Jagid J, Maudsley AA.
"These results demonstrate that significant and widespread alterations of brain metabolites occur as a result of mild-to-moderate TBI, and that these measures correlate with measures of cognitive performance."
where
http://www.ncbi.nlm.nih.gov/pubmed/20201668

Understanding the neuroinflammatory response following concussion to develop treatment strategies. 2012
Patterson ZR, Holahan MR.
"Mild traumatic brain injuries (mTBI) have been associated with long-term cognitive deficits relating to trauma-induced neurodegeneration. These long-term deficits include impaired memory and attention, changes in executive function, emotional instability, and sensorimotor deficits. Furthermore, individuals with concussions show a high co-morbidity with a host of psychiatric illnesses (e.g., depression, anxiety, addiction) and dementia. The neurological damage seen in mTBI patients is the result of the impact forces and mechanical injury, followed by a delayed neuroimmune response that can last hours, days, and even months after the injury."
Department of Neuroscience, Carleton University Ottawa, ON, Canada.
http://www.ncbi.nlm.nih.gov/pubmed/23248582