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Genetics traumatic brain injury

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https://www.readbyqxmd.com/read/29770117/clinical-application-of-epilepsy-genetics-in-africa-is-now-the-time
#1
Alina I Esterhuizen, Gemma L Carvill, Rajkumar S Ramesar, Symon M Kariuki, Charles R Newton, Annapurna Poduri, Jo M Wilmshurst
Over 80% of people with epilepsy live in low- to middle-income countries where epilepsy is often undiagnosed and untreated due to limited resources and poor infrastructure. In Africa, the burden of epilepsy is exacerbated by increased risk factors such as central nervous system infections, perinatal insults, and traumatic brain injury. Despite the high incidence of these etiologies, the cause of epilepsy in over 60% of African children is unknown, suggesting a possible genetic origin. Large-scale genetic and genomic research in Europe and North America has revealed new genes and variants underlying disease in a range of epilepsy phenotypes...
2018: Frontiers in Neurology
https://www.readbyqxmd.com/read/29768967/interleukin-1-receptor-1-deletion-in-focal-and-diffuse-experimental-traumatic-brain-injury-in-mice
#2
Joon Yong Chung, Nicolas Krapp, Limin Wu, Sevda Lule, Lauren McAllister, William Edmiston Iii, Samantha Martin, Emily Levy, Tanya Songtachalert, John Sherwood, Erin Buckley, Bharat Sanders, Saef Izzy, Suzanne Hickman, Shuzhen Guo, Josephine Lok, Joseph El Khoury, Eng Lo, David Kaplan, Michael Whalen
Important differences in the biology of focal and diffuse traumatic brain injury (TBI) subtypes may result in unique pathophysiological responses to shared molecular mechanisms. Interleukin-1 (IL-1) signaling has been tested as a potential therapeutic target in preclinical models of cerebral contusion and diffuse TBI, and in a phase II clinical trial, but no published studies have examined IL-1 signaling in an impact/acceleration closed head injury (CHI) model. We hypothesized that genetic deletion of IL-1 receptor-1 (IL-1R1 KO) would be beneficial in focal (contusion) and CHI in mice...
May 17, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29717626/the-moderating-effect-of-ankk1-on-the-association-of-family-environment-with-longitudinal-executive-function-following-traumatic-brain-injury-in-early-childhood-a-preliminary-study
#3
Julia Smith-Paine, Shari L Wade, Amery Treble-Barna, Nanhua Zhang, Huaiyu Zang, Lisa J Martin, Keith Owen Yeates, H Gerry Taylor, Brad G Kurowski
This study examined whether the ankyrin repeat and kinase domain containing 1 gene (ANKK1) C/T single-nucleotide polymorphism (SNP) rs1800497 moderated the association of family environment with long-term executive function (EF) following traumatic injury in early childhood. Caregivers of children with traumatic brain injury (TBI) and children with orthopedic injury (OI) completed the Behavior Rating Inventory of Executive Function (BRIEF) at post injury visits. DNA was collected to identify the rs1800497 genotype in the ANKK1 gene...
May 2, 2018: Journal of Neurotrauma
https://www.readbyqxmd.com/read/29710079/neurobiology-of-opioid-use-disorder-and-comorbid-traumatic-brain-injury
#4
Thomas R Kosten, David P Graham, David A Nielsen
Importance: Treating patients with opioid use disorder (OUD) and traumatic brain injury illustrates 6 neurobiological principles about the actions of 2 contrasting opioid analgesics, morphine and fentanyl, as well as pharmacotherapies for OUD, methadone, naltrexone, and buprenorphine. Observations: This literature review focused on a patient with traumatic brain injury who developed OUD from chronic morphine analgesia. His treatment is described in a neurobiological framework of 6 opioid action principles...
April 25, 2018: JAMA Psychiatry
https://www.readbyqxmd.com/read/29707426/is-electroconvulsive-therapy-a-treatment-for-depression-following-traumatic-brain-injury
#5
Anja Srienc, Puneet Narang, Simrat Sarai, Yee Xiong, Steven Lippmann
Traumatic brain injury (TBI) can be caused by blunt or penetrating injury to the head. The pathophysiological evolution of TBI involves complex biochemical and genetic changes. Common sequelae of TBI include seizures and psychiatric disorders, particularly depression. In considering pharmacologic interventions for treating post-TBI depression, it is important to remember that TBI patients have a higher risk of seizures; therefore, the benefits of prescribing medications that lower the seizure threshold need to be weighed against the risk of seizures...
April 1, 2018: Innovations in Clinical Neuroscience
https://www.readbyqxmd.com/read/29688987/reduction-in-blood-glutamate-levels-combined-with-the-genetic-inactivation-of-a2ar-significantly-alleviate-traumatic-brain-injury-induced-acute-lung-injury
#6
Wei Bai, Ping Li, Ya-Lei Ning, Yu-Lin Jiang, Nan Yang, Xing Chen, Yuan-Guo Zhou
Traumatic brain injury-induced acute lung injury (TBI-ALI) is a serious complication of traumatic brain injury (TBI). Our previous clinical study found that high levels of blood glutamate after TBI were closely related to the occurrence and severity of TBI-ALI, while it remains unknown whether a high concentration of blood glutamate directly causes or aggravates TBI-ALI. We found that inhibition of the adenosine A2A receptor (A2AR) after brain injury alleviated the TBI-ALI; however, it is unknown whether lowering blood glutamate levels in combination with inhibiting the A2AR would lead to better effects...
April 23, 2018: Shock
https://www.readbyqxmd.com/read/29682502/frontiers-of-complex-disease-mechanisms-membrane-surface-tension-may-link-genotype-to-phenotype-in-glaucoma
#7
Howard R Petty
Although many monogenic diseases are understood based upon structural changes of gene products, less progress has been made concerning polygenic disease mechanisms. This article presents a new interdisciplinary approach to understand complex diseases, especially their genetic polymorphisms. I focus upon primary open angle glaucoma (POAG). Although elevated intraocular pressure (IOP) and oxidative stress are glaucoma hallmarks, the linkages between these factors and cell death are obscure. Reactive oxygen species (ROS) promote the formation of oxidatively truncated phosphoglycerides (OTP), free fatty acids, lysophosphoglycerides, oxysterols, and other chemical species that promote membrane disruption and decrease membrane surface tension...
2018: Frontiers in Cell and Developmental Biology
https://www.readbyqxmd.com/read/29663285/exosomes-in-acquired-neurological-disorders-new-insights-into-pathophysiology-and-treatment
#8
REVIEW
Nicole Osier, Vida Motamedi, Katie Edwards, Ava Puccio, Ramon Diaz-Arrastia, Kimbra Kenney, Jessica Gill
Exosomes are endogenous nanovesicles that play critical roles in intercellular signaling by conveying functional genetic information and proteins between cells. Exosomes readily cross the blood-brain barrier and have promise as therapeutic delivery vehicles that have the potential to specifically deliver molecules to the central nervous system (CNS). This unique feature also makes exosomes attractive as biomarkers in diagnostics, prognostics, and therapeutics in the context of multiple significant public health conditions, including acquired neurological disorders...
April 16, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29662944/combined-blockade-of-interleukin-1%C3%AE-and-1%C3%AE-signaling-protects-mice-from-cognitive-dysfunction-after-traumatic-brain-injury
#9
Elizabeth A Newell, Brittany P Todd, Jolonda Mahoney, Andrew A Pieper, Polly J Ferguson, Alexander G Bassuk
Diffuse activation of interleukin-1 inflammatory cytokine signaling after traumatic brain injury (TBI) elicits progressive neurodegeneration and neuropsychiatric dysfunction, and thus represents a potential opportunity for therapeutic intervention. Although interleukin (IL)-1α and IL-1β both activate the common type 1 IL-1 receptor (IL-1RI), they manifest distinct injury-specific roles in some models of neurodegeneration. Despite its potential relevance to treating patients with TBI, however, the individual contributions of IL-1α and IL-1β to TBI-pathology have not been previously investigated...
March 2018: ENeuro
https://www.readbyqxmd.com/read/29614682/non-genetic-risk-factors-for-degenerative-and-vascular-young-onset-dementia-results-from-the-inspired-and-kgow-studies
#10
Monica Cations, Brian Draper, Lee-Fay Low, Kylie Radford, Julian Trollor, Henry Brodaty, Perminder Sachdev, Peter Gonski, Gerald Anthony Broe, Adrienne Withall
BACKGROUND: Several brain reserve, vascular risk, and other modifiable factors have been associated with late-onset dementia, but their association with young onset dementia (YOD) has not been adequately explored. OBJECTIVE: To examine the association of cognitive reserve enhancing factors, cardiovascular risk factors (including smoking), depression, alcohol use, and traumatic brain injury (TBI) with non-autosomal dominant degenerative and/or vascular YOD. METHODS: Data for this matched case-control study were taken from two larger studies conducted in NSW, Australia...
2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29614674/optical-depolarization-of-dcx-expressing-cells-promoted-cognitive-recovery-and-maturation-of-newborn-neurons-via-the-wnt-%C3%AE-catenin-pathway
#11
Ming-Liang Zhao, Shi-Jin Chen, Xiao-Hong Li, Li-Na Wang, Feng Chen, Shi-Jiang Zhong, Cheng Yang, Sheng-Kai Sun, Jian-Jun Li, Hua-Jiang Dong, Yue-Qing Dong, Yi Wang, Chong Chen
Electrical excitability by membrane depolarization is crucial for survival and maturation of newborn cells in the dentate gyrus of the hippocampus. However, traditional technology for membrane depolarization lacks temporal and spatial precision. Optogenetics can be used to activate channelrhodopsin-2 (ChR2), allowing cationic current to depolarize genetically targeted cells. In this study, we used ChR2-EGFP driven by doublecortin (DCX) to promote survival and maturation of newborn cells in the dentate gyrus after traumatic brain injury (TBI)...
March 28, 2018: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29605745/phenotypic-spectrum-in-families-with-mesial-temporal-lobe-epilepsy-probands
#12
Emilija Cvetkovska, Igor Kuzmanovski, Marija Babunovska, Bojan Boshkovski, Tatjana Cepreganova Cangovska, Gordana Kiteva Trencevska
PURPOSE: The traditional perception of mesial temporal lobe epilepsy (MTLE) as a predominantly acquired disorder is challenged due to emerging evidence of familial aggregation. In this study, we ascertained the extent of familial occurrence of epilepsy in MTLE patients, as well as phenotypic heterogeneity in affected relatives. METHODS: We identified and reevaluated patients with MTLE, treated at Epilepsy Department for a period of two years. All eligible putatively affected relatives were asked to participate in the study...
March 27, 2018: Seizure: the Journal of the British Epilepsy Association
https://www.readbyqxmd.com/read/29574129/activity-dependent-internalization-of-the-glutamate-transporter-glt-1-requires-calcium-entry-through-the-ncx-sodium-calcium-exchanger
#13
Ignacio Ibáñez, David Bartolomé-Martín, Dolores Piniella, Cecilio Giménez, Francisco Zafra
GLT-1 is the main glutamate transporter in the brain and its trafficking controls its availability at the cell surface, thereby shaping glutamatergic neurotransmission under physiological and pathological conditions. Extracellular glutamate is known to trigger ubiquitin-dependent GLT-1 internalization from the surface of the cell to the intracellular compartment, yet here we show that internalization also requires the participation of calcium ions. Consistent with previous studies, the addition of glutamate (1 mM) to mixed primary cultures (containing neurons and astrocytes) promotes GLT-1 internalization, an effect that was suppressed in the absence of extracellular Ca2+ ...
March 21, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29568799/susceptibility-to-oxidative-stress-is-determined-by-genetic-background-in-neuronal-cell-cultures
#14
Mattias Günther, Faiez Al Nimer, Fredrik Piehl, Mårten Risling, Tiit Mathiesen
Traumatic brain injury (TBI) leads to a deleterious and multifactorial secondary inflammatory response in the brain. Oxidative stress from the inflammation likely contributes to the brain damage although it is unclear to which extent. A largely unexplored approach is to consider phenotypic regulation of oxidative stress levels. Genetic polymorphism influences inflammation in the central nervous system and it is possible that the antioxidative response differs between phenotypes and affects the severity of the secondary injury...
March 2018: ENeuro
https://www.readbyqxmd.com/read/29567804/primary-traumatic-axonopathy-in-mice-subjected-to-impact-acceleration-a-reappraisal-of-pathology-and-mechanisms-with-high-resolution-anatomical-methods
#15
Nikolaos K Ziogas, Vassilis E Koliatsos
Traumatic axonal injury (TAI) is a common neuropathology in traumatic brain injury (TBI) and is featured by primary injury to axons. Here, we generated TAI with impact acceleration of the head (IA) in male Thy1-eYFP-H transgenic mice in which specific populations of neurons and their axons are labeled with yellow fluorescent protein (YFP). This model results in axonal lesions in multiple axonal tracts along with blood brain barrier (BBB) disruption and neuroinflammation. The corticospinal tract (CST), a prototypical long tract, is severely affected and is the focus of this study...
March 22, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29556212/long-term-consequences-of-traumatic-brain-injury-in-bone-metabolism
#16
REVIEW
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
https://www.readbyqxmd.com/read/29463164/apolipoprotein-e-apoe-%C3%AE%C2%B54-genotype-is-associated-with-elevated-psychiatric-distress-in-veterans-with-a-history-of-mild-to-moderate-traumatic-brain-injury
#17
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
https://www.readbyqxmd.com/read/29458437/ablation-of-caspase-1-protects-against-tbi-induced-pyroptosis-in-vitro-and-in-vivo
#18
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
https://www.readbyqxmd.com/read/29432563/traumatic-injury-induces-stress-granule-formation-and-enhances-motor-dysfunctions-in-als-ftd-models
#19
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 whether 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...
April 15, 2018: Human Molecular Genetics
https://www.readbyqxmd.com/read/29422364/glioblastoma-arising-within-sites-of-encephalomalacia-from-cerebrovascular-insult-two-cases-and-a-review-of-the-literature
#20
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...
April 2018: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
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