Cellular and Molecular Mechanisms of Secondary Neuronal Injury following Traumatic Brain Injury

Krishnamurthy, Kamesh; Laskowitz, Daniel T.

doi:10.1201/b18959-10

Cited by 30 publications

(31 citation statements)

References 1 publication

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“…Concussion risk is more likely explained by a polygenetic relationship 70. The potential genetic predisposition to chronic traumatic encephalopathy (CTE) is the subject of several large studies, with one hypothesis being that genetic factors may modulate the environmental effects of repetitive traumatic collisions to the head 71…”

Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms associated with the risk of concussion in 1056 college athletes: a multicentre prospective cohort study

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Genetic polymorphisms associated with the risk of concussion in 1056 college athletes: a multicentre prospective cohort study

et al. 2017

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“…Single nucleotide polymorphism (SNP) refers to a difference in single DNA building block of a gene (nucleotide) or within the regulatory regions of a gene. SNPs are the most common type of genetic variations among people and occur once in every 100–300 nucleotides; there are roughly 10 million SNPs in the human genome . SNPs can be used as a biomarker for predicting an individual's risk to the disease, response to certain drugs, susceptibility to environmental factors and to track the inheritance of disease genes within families …”

Section: Lncrna Snps In Cancer Risk Predictionmentioning

confidence: 99%

“…SNPs are the most common type of genetic variations among people and occur once in every 100-300 nucleotides; there are roughly 10 million SNPs in the human genome. 118 SNPs can be used as a biomarker for predicting an individual's risk to the disease, response to certain drugs, susceptibility to environmental factors and to track the inheritance of disease genes within families. 119 A number of cancer associated SNPs have been identified in the past, majority of which map to the non-coding regions.…”

Section: Lncrna Snps In Cancer Risk Predictionmentioning

confidence: 99%

Potential of long non‐coding RNAs in cancer patients: From biomarkers to therapeutic targets

Gupta

Tripathi

2016

Intl Journal of Cancer

420

260

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Because of high specificity and easy detection in the tissues, serum, plasma, urine and saliva, interest in exploring the potential of long non-coding RNAs (lncRNAs) in cancer patients continues to increase. LncRNAs have shown potential as a biomarker in the diagnosis and prognosis of bladder cancer, prostate cancer, gastric cancer, pancreatic cancer, breast cancer and many other cancer types. Some lncRNAs have also been used as adjunct to improve the specificity and sensitivity of existing biomarkers. The molecular tools such as RNA-seq, RNA-FISH, ic-SHAPE and quantitative real-time PCR have been used for examining the lncRNAs' potential. Some lncRNAs such as PCA3 is now routinely used in the clinic for the diagnosis of prostate cancer. Single nucleotide polymorphisms (SNPs) in lncRNAs can also be used as a predictor of cancer risk. Although ongoing studies continue to unravel the underlying mechanism, some lncRNAs have been used as therapeutic targets for the selective killing of cancer cells in patients. Thus lncRNAs are emerging as convenient and minimally invasive diagnostic/prognostic markers, and also as therapeutic target. Companies such as the Curna Inc., MiNA Therapeutics Ltd. and RaNA Therapeutics Inc. have been taking steps to develop lncRNA based strategies against cancer. In this review, we discuss the potential of lncRNAs as biomarkers and therapeutic targets in cancer patients.

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“…With regard to the identification of specific genetic variants associated with the development of epilepsy following brain injury in humans, most findings come from studies of TBI. A recent review by Bennett et al summarizes the results of 31 separate studies describing polymorphisms in 24 genes, including genes involved in the inflammatory response (eg, pro‐ and anti‐inflammatory cytokines such as tumor necrosis factor [TNF]‐α and interleukin [IL]‐6), neuronal plasticity (eg, brain‐derived neurotrophic factor [BDNF]), and cognitive function (eg, catechol‐O‐methyl transferase). Some of these genes are of particular interest given the roles of inflammatory factors and growth factors in epileptogenesis .…”

Section: Genetic Aspects In Patientsmentioning

confidence: 99%

Commonalities in epileptogenic processes from different acute brain insults: Do they translate?

et al. 2017

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Summary The most common forms of acquired epilepsies arise following acute brain insults such as traumatic brain injury, stroke, or central nervous system infections. Treatment is effective for only 60%‐70% of patients and remains symptomatic despite decades of effort to develop epilepsy prevention therapies. Recent preclinical efforts are focused on likely primary drivers of epileptogenesis, namely inflammation, neuron loss, plasticity, and circuit reorganization. This review suggests a path to identify neuronal and molecular targets for clinical testing of specific hypotheses about epileptogenesis and its prevention or modification. Acquired human epilepsies with different etiologies share some features with animal models. We identify these commonalities and discuss their relevance to the development of successful epilepsy prevention or disease modification strategies. Risk factors for developing epilepsy that appear common to multiple acute injury etiologies include intracranial bleeding, disruption of the blood‐brain barrier, more severe injury, and early seizures within 1 week of injury. In diverse human epilepsies and animal models, seizures appear to propagate within a limbic or thalamocortical/corticocortical network. Common histopathologic features of epilepsy of diverse and mostly focal origin are microglial activation and astrogliosis, heterotopic neurons in the white matter, loss of neurons, and the presence of inflammatory cellular infiltrates. Astrocytes exhibit smaller K+ conductances and lose gap junction coupling in many animal models as well as in sclerotic hippocampi from temporal lobe epilepsy patients. There is increasing evidence that epilepsy can be prevented or aborted in preclinical animal models of acquired epilepsy by interfering with processes that appear common to multiple acute injury etiologies, for example, in post–status epilepticus models of focal epilepsy by transient treatment with a trkB/PLCγ1 inhibitor, isoflurane, or HMGB1 antibodies and by topical administration of adenosine, in the cortical fluid percussion injury model by focal cooling, and in the albumin posttraumatic epilepsy model by losartan. Preclinical studies further highlight the roles of mTOR1 pathways, JAK‐STAT3, IL‐1R/TLR4 signaling, and other inflammatory pathways in the genesis or modulation of epilepsy after brain injury. The wealth of commonalities, diversity of molecular targets identified preclinically, and likely multidimensional nature of epileptogenesis argue for a combinatorial strategy in prevention therapy. Going forward, the identification of impending epilepsy biomarkers to allow better patient selection, together with better alignment with multisite preclinical trials in animal models, should guide the clinical testing of new hypotheses for epileptogenesis and its prevention.

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Cellular and Molecular Mechanisms of Secondary Neuronal Injury following Traumatic Brain Injury

Cited by 30 publications

References 1 publication

Genetic polymorphisms associated with the risk of concussion in 1056 college athletes: a multicentre prospective cohort study

Genetic polymorphisms associated with the risk of concussion in 1056 college athletes: a multicentre prospective cohort study

Potential of long non‐coding RNAs in cancer patients: From biomarkers to therapeutic targets

Commonalities in epileptogenic processes from different acute brain insults: Do they translate?

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