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Genetics traumatic brain injury

Nikita M Bajwa, Chandrasekhar Kesavan, Subburaman Mohan
Traumatic brain injury (TBI) leads to long-term cognitive, behavioral, affective deficits, and increase neurodegenerative diseases. It is only in recent years that there is growing awareness that TBI even in its milder form poses long-term health consequences to not only the brain but to other organ systems. Also, the concept that hormonal signals and neural circuits that originate in the hypothalamus play key roles in regulating skeletal system is gaining recognition based on recent mouse genetic studies. Accordingly, many TBI patients have also presented with hormonal dysfunction, increased skeletal fragility, and increased risk of skeletal diseases...
2018: Frontiers in Neurology
Victoria C Merritt, Alexandra L Clark, Scott F Sorg, Nicole D Evangelista, Madeleine Werhane, Mark W Bondi, Dawn M Schiehser, Lisa Delano-Wood
Since few studies have examined the relationship between the APOE gene and clinical outcomes following military-related traumatic brain injury (TBI), we aimed to determine whether the ε4 allele of the APOE gene influences neuropsychiatric symptoms in Veterans with a history of mild to moderate TBI. Participants included 133 Veterans (TBI=79, military controls [MC]=54) who underwent APOE genotyping and were divided into ε4+ (TBI=18, MC=15) and ε4- (TBI=61, MC=39) groups. All participants underwent evaluation of psychological distress using the Beck Depression Inventory-II (BDI-II), Beck Anxiety Inventory (BAI), and PTSD Checklist-Military Version (PCL-M)...
February 20, 2018: Journal of Neurotrauma
Wei Liu, Yuhua Chen, Jiao Meng, Minfei Wu, Fangfang Bi, Cuicui Chang, Hua Li, Liangjun Zhang
BACKGROUND: Traumatic brain injury (TBI) is a critical public health and socioeconomic problem throughout the world. Inflammation-induced secondary injury is one of the vital pathogenic parameters of TBI. Molecular signaling cascades of pyroptosis, a specific type of cellular necrosis, are key drivers of TBI-induced inflammation. METHODS: In this study, mice with genetically ablated caspase-1 (caspase-1-/- ) were subjected to controlled cortical impact injury in vivo, and primary neuron deficient in caspase-1 through siRNA knockdown and pharmacologic inhibition was stimulated by mechanical scratch, equiaxial stretch, and LPS/ATP in vitro...
February 19, 2018: Journal of Neuroinflammation
Eric N Anderson, Lauren Gochenaur, Aditi Singh, Rogan Grant, Krishani Patel, Simon Watkins, Jane Y Wu, Udai Bhan Pandey
Traumatic brain injury (TBI) has been predicted to be a predisposing factor for Amyotrophic lateral sclerosis (ALS) and other neurological disorders. Despite the importance of TBI in ALS progression, the underlying cellular and molecular mechanisms are still an enigma. Here, we examined the contribution of TBI as an extrinsic factor and investigated if TBI influences the susceptibility of developing neurodegenerative symptoms. To evaluate the effects of TBI in vivo, we applied mild to severe trauma to Drosophila and found that TBI leads to the induction of stress granules (SGs) in the brain...
February 8, 2018: Human Molecular Genetics
Emily A Ferenczi, Altaf Saadi, Shamik Bhattacharyya, Aaron L Berkowitz
Glioblastoma is the most common primary parenchymal brain malignancy, with median survival of less than one year. While there are likely multiple predisposing genetic and environmental factors in glioblastoma formation, chronic inflammation resulting from non-traumatic vascular brain injury is one proposed risk factor for oncogenesis. Here, we report two instances of glioblastoma arising within areas of encephalomalacia caused by remote vascular insults (one following aneurysmal subarachnoid hemorrhage and one following ischemic infarction), review the literature associating glioblastoma with prior brain injury, and discuss potential mechanisms for malignant transformation in injured brain tissue...
February 5, 2018: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
Elliott Jay Mufson, Bin He, Stephen D Ginsberg, Benjamin A Carper, Gayle S Bieler, Fiona C Crawford, Victor E Alverez, Bernard R Huber, Thor D Stein, Ann C McKee, Sylvia E Perez
Military personnel and athletes exposed to traumatic brain injury may develop chronic traumatic encephalopathy (CTE). Brain pathology in CTE includes intracellular accumulation of abnormally phosphorylated tau proteins (p-tau), the main constituent of neurofibrillary tangles (NFTs). Recently, we found that cholinergic basal forebrain (CBF) neurons within the nucleus basalis of Meynert (nbM), which provide the major cholinergic innervation to the cortex, display an increasing number of NFTs across the pathological stages of CTE...
January 16, 2018: Journal of Neurotrauma
Alicia G Kachmar, Sharon Y Irving, Cynthia A Connolly, Martha A Q Curley
OBJECTIVES: To identify risk factors associated with cognitive impairment as assessed by neuropsychologic tests in neurotypical children after critical illness. DATA SOURCES: For this systematic review, we searched the Cochrane Library, Scopus, PubMed, Ovid, Embase, and CINAHL databases from January 1960 to March 2017. STUDY SELECTION: Included were studies with subjects 3-18 years old at the time of post PICU follow-up evaluation and use of an objective standardized neuropsychologic test with at least one cognitive functioning dimension...
January 11, 2018: Pediatric Critical Care Medicine
Amanda L Maheras, Brian Dix, Olivia M S Carmo, Aleena E Young, Vanessa N Gill, Julia L Sun, Aleah R Booker, Helen A Thomason, Anastasia E Ibrahim, Lauren Stanislaw, Jennifer C Dallego, Cat N Ngo, Audrey Chen, Barbara K Fortini, Rory D Spence
Mild traumatic brain injuries (mTBIs) are one of the most prevalent neurological disorders, and humans are severely limited in their ability to repair and regenerate central nervous system (CNS) tissue postinjury. However, zebrafish (Danio rerio) maintain the remarkable ability to undergo complete and functional neuroregeneration as an adult. We wish to extend knowledge of the known mechanisms of neuroregeneration by analyzing the differentially expressed genes (DEGs) in a novel adult zebrafish model of mTBI...
January 2018: ENeuro
Patrick E Georgoff, Vahagn C Nikolian, Gerald Higgins, Kiril Chtraklin, Hassan Eidy, Mohamed H Ghandour, Aaron Williams, Brian Athey, Hasan B Alam
BACKGROUND: Valproic acid (VPA) is a histone deacetylase inhibitor that improves outcomes in large animal models of trauma. However, its protective mechanism of action is not completely understood. We sought to characterize the genetic changes induced by VPA treatment following traumatic injuries. METHODS: Six female Yorkshire swine were subjected to traumatic brain injury (TBI, controlled cortical impact), polytrauma (liver and splenic laceration, rib fracture, rectus crush), and hemorrhagic shock (HS, 40% total blood volume)...
December 14, 2017: Journal of Trauma and Acute Care Surgery
Jing Chen, Wanwan He, Xu Hu, Yuwen Shen, Junyan Cao, Zhengdong Wei, Yifei Luan, Li He, Fangdun Jiang, Yanmei Tao
Reactive astrogliosis is a hallmark of many neurological disorders, yet its functions and molecular mechanisms remain elusive. Particularly, the upstream signaling that regulates pathological responses of astrocytes is largely undetermined. We used a mouse traumatic brain injury model to induce astrogliosis and revealed activation of ErbB receptors in reactive astrocytes. Moreover, cell-autonomous inhibition of ErbB receptor activity in reactive astrocytes by a genetic approach suppressed hypertrophic remodeling possibly through the regulation of actin dynamics...
2017: Cell Discovery
Eric J Neuberger, Akshay Gupta, Deepak Subramanian, Akshata A Korgaonkar, Vijayalakshmi Santhakumar
Epilepsy, characterized by recurrent seizures and abnormal electrical activity in the brain, is one of the most prevalent brain disorders. Over two million people in the United States have been diagnosed with epilepsy and 3% of the general population will be diagnosed with it at some point in their lives. While most developmental epilepsies occur due to genetic predisposition, a class of "acquired" epilepsies results from a variety of brain insults. A leading etiological factor for epilepsy that is currently on the rise is traumatic brain injury (TBI), which accounts for up to 20% of all symptomatic epilepsies...
November 29, 2017: Journal of Neuroscience Research
Arko Sen, Katherine Gurdziel, Jenney Liu, Wen Qu, Oluwademi O Nuga, Rayanne B Burl, Maik Hüttemann, Roger Pique-Regi, Douglas M Ruden
Traumatic brain injury (TBI) can cause persistent pathological alteration of neurons. This may lead to cognitive dysfunction, depression and increased susceptibility to life threatening diseases, such as epilepsy and Alzheimer's disease. To investigate the underlying genetic and molecular basis of TBI, we subjected w 1118 Drosophila melanogaster to mild closed head trauma and found that mitochondrial activity is reduced in the brains of these flies 24 h after inflicting trauma. To determine the transcriptomic changes after mild TBI, we collected fly heads 24 h after inflicting trauma, and performed RNA-seq analyses...
2017: Frontiers in Genetics
Kimbra Kenney, Diego Iacono, Brian L Edlow, Douglas I Katz, Ramon Diaz-Arrastia, Kristen Dams-O'Connor, Daniel H Daneshvar, Allison Stevens, Allison L Moreau, Lee S Tirrell, Ani Varjabedian, Anastasia Yendiki, Andre van der Kouwe, Azma Mareyam, Jennifer A McNab, Wayne A Gordon, Bruce Fischl, Ann C McKee, Daniel P Perl
We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). Neuropathological evaluation revealed abundant β-amyloid neuritic and cored plaques, diffuse β-amyloid plaques, and frequent hyperphosphorylated-tau neurofibrillary tangles (NFT) involving much of the cortex, including insula and mammillary bodies in both cases. Case 1 additionally showed NFTs in both the superficial and deep cortical layers, occasional perivascular and depth-of-sulci NFTs, and parietal white matter rarefaction, which corresponded with decreased parietal fiber tracts observed on ex vivo MRI...
November 16, 2017: Journal of Neuropathology and Experimental Neurology
Jean-Pierre Dollé, Andrew Jaye, Stewart A Anderson, Hossein Ahmadzadeh, Vivek B Shenoy, Douglas H Smith
Since traumatic axonal injury (TAI) is implicated as a prominent pathology of concussion, we examined potential sex differences in axon structure and responses to TAI. Rat and human neurons were used to develop micropatterned axon tracts in vitro that were genetically either male or female. Ultrastructural analysis revealed for the first time that female axons were consistently smaller with fewer microtubules than male axons. Computational modeling of TAI showed that these structural differences place microtubules in female axons at greater risk of failure during trauma under the same applied loads than in male axons...
February 2018: Experimental Neurology
Aleksandra Gilis-Januszewska, Łukasz Kluczyński, Małgorzata Wilusz, Jacek Pantofliński, Renata Turek-Jabrocka, Dorota Pach, Alicja Hubalewska-Dydejczyk
RATIONALE: Traumatic thoracic injuries in adolescents are rare but could be connected with traumatic brain injuries (TBI) and development of chronic hypopituitarism. Early recognition of these endocrine problems is a significant challenge to clinicians. We present difficulties in diagnosis of hypothalamic-pituitary insufficiency following traumatic thoracic injury in adolescence. We also review the literature of similar cases. PATIENT CONCERNS: We present a case of a 24-years-old male...
November 2017: Medicine (Baltimore)
Raghavendar Chandran, TaeHee Kim, Suresh L Mehta, Eshwar Udho, Vishal Chanana, Pelin Cengiz, HwuiWon Kim, Chanul Kim, Raghu Vemuganti
Uncontrolled oxidative stress contributes to the secondary neuronal death that promotes long-term neurological dysfunction following traumatic brain injury (TBI). Surprisingly, both NADPH oxidase 2 (NOX2) that increases and transcription factor Nrf2 that decreases reactive oxygen species (ROS) are induced after TBI. As the post-injury functional outcome depends on the balance of these opposing molecular pathways, we evaluated the effect of TBI on the motor and cognitive deficits and cortical contusion volume in NOX2 and Nrf2 knockout mice...
January 1, 2017: Journal of Cerebral Blood Flow and Metabolism
Genevieve M Sullivan, Regina C Armstrong
Neural stem cells (NSCs) delivered intraventricularly may be therapeutic for diffuse white matter pathology after traumatic brain injury (TBI). To test this concept, NSCs isolated from adult mouse subventricular zone (SVZ) were transplanted into the lateral ventricle of adult mice at two weeks post-TBI followed by analysis at four weeks post-TBI. We examined sonic hedgehog (Shh) signaling as a candidate mechanism by which transplanted NSCs may regulate neuroregeneration and/or neuroinflammation responses of endogenous cells...
2017: Stem Cells International
Claire Jourdan, Philippe Azouvi, François Genêt, Nicolas Selly, Loic Josseran, Alexis Schnitzler
OBJECTIVE: To measure the prevalence of traumatic brain injury-related disability and health status in the general population. DESIGN: The French National Survey, conducted in households and institutions, assessed 33,896 adults. Data included sequelae from traumatic brain injury, impairments, current health conditions and uses of health services. Analyses, adjusted for age and gender, compared subjects who declared sequelae from traumatic brain injury (n=479) to the remaining survey population (n=33,287)...
October 7, 2017: American Journal of Physical Medicine & Rehabilitation
Solomon M Adams, Yvette P Conley, Amy K Wagner, Ruchira M Jha, Robert Sb Clark, Samuel M Poloyac, Patrick M Kochanek, Philip E Empey
Pharmacotherapy for traumatic brain injury (TBI) is focused on resuscitation, prevention of secondary injury, rehabilitation and recovery. Pharmacogenomics may play a role in TBI for predicting therapies for sedation, analgesia, seizure prevention, intracranial pressure-directed therapy and neurobehavioral/psychiatric symptoms. Research into genetic predictors of outcomes and susceptibility to complications may also help clinicians to tailor therapeutics for high-risk individuals. Additionally, the expanding use of genomics in the drug development pipeline has provided insight to novel investigational and repurposed medications that may be useful in the treatment of TBI and its complications...
October 2017: Pharmacogenomics
Jing Wang, Merry W Ma, Krishnan M Dhandapani, Darrell W Brann
Traumatic brain injury (TBI) is a leading cause of death and disability. Secondary injuries that develop after the initial trauma contribute to long-lasting neurophysiological deficits. Polarization of microglia/macrophages toward a pro-inflammatory (M1) phenotype may increase the progression of secondary injury following TBI; however, the regulatory and functional mechanisms underlying these changes remain poorly defined. In the present study, we showed elevated expression of NADPH oxidase 2 (NOX2) and activation of nuclear factor-kappa B (NF-κB) predominantly in microglia/macrophages at 4- and 7-days after controlled cortical impact in mice...
September 21, 2017: Free Radical Biology & Medicine
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