Genetic Factors in Alcohol Abuse: Animal Models

1983 ◽  
pp. 1-30 ◽  
Author(s):  
Gerald E. McClearn
Keyword(s):  
Animal Models ◽  
Alcohol Abuse ◽  
Genetic Factors

Advances in Our Understanding of Dystonia - Pathophysiology and Treatment Options

2011 ◽  
Vol 6 (2) ◽  
pp. 121 ◽  
Author(s):  
Naomi Lubarr ◽  
Susan Bressman ◽  
◽  
Keyword(s):  
Animal Models ◽  
Genetic Factors ◽  
Functional Neuroimaging ◽  
Treatment Options ◽  
Motor Dysfunction ◽  
Complete Understanding ◽  
Multiple Points ◽  
Second Hit ◽  
The Past ◽  
Similar Motor

Although the pathophysiology of dystonia remains incompletely understood, advances in two major areas of research over the past two decades have led to important insights into the mechanisms of dystonia. First, with the identification of dystonia genes, investigations using cellular and animal models of dystonia have become possible. Second, advances in functional neuroimaging have led to the possibility of identification of distinct functional, anatomical and neurochemical abnormalities in dystonia patients. Dystonia is currently conceptualised as a neurofunctional disorder characterised by alterations at various levels and multiple points along the sensorimotor circuit. There are multiple causes of these disruptions, and lesions along different points in interconnected pathways can yield similar motor dysfunction. The existence of dystonia endophenotypes in genetic forms of dystonia suggests that it may be a ‘second hit’ disorder, in which genetically predisposed brains can be thrown into an unbalanced dystonic state by environmental or genetic factors. Ultimately, a more complete understanding of the pathophysiology of dystonia should lead to better, more rational, targeted therapies.

scholarly journals CNS autoimmune disease afterStreptococcus pyogenesinfections: animal models, cellular mechanisms and genetic factors

2016 ◽  
Vol 11 (1) ◽  
pp. 63-76 ◽  
Author(s):  
Tyler Cutforth ◽  
Mellissa MC DeMille ◽  
Ilir Agalliu ◽  
Dritan Agalliu
Keyword(s):  
Autoimmune Disease ◽  
Animal Models ◽  
Genetic Factors ◽  
Cellular Mechanisms

scholarly journals Animal models for medications development targeting alcohol abuse using selectively bred rat lines: Neurobiological and pharmacological validity

2012 ◽  
Vol 103 (1) ◽  
pp. 119-155 ◽  
Author(s):  
Richard L. Bell ◽  
Helen J.K. Sable ◽  
Giancarlo Colombo ◽  
Petri Hyytia ◽  
Zachary A. Rodd ◽  
...  
Keyword(s):  
Animal Models ◽  
Alcohol Abuse

scholarly journals Trigeminal neuralgia and genetics: A systematic review

2021 ◽  
Vol 17 ◽  
pp. 174480692110161
Author(s):  
Mari Aaroe Mannerak ◽  
Aslan Lashkarivand ◽  
Per Kristian Eide
Keyword(s):  
Systematic Review ◽  
Animal Models ◽  
Trigeminal Neuralgia ◽  
Animal Studies ◽  
Genetic Factors ◽  
Web Of Science ◽  
Cochrane Library ◽  
Trigeminal Pain ◽  
Familial Form

Trigeminal neuralgia (TN) is a severe facial pain disease of unknown cause and unclear genetic background. To examine the existing knowledge about genetics in TN, we performed a systematic study asking about the prevalence of familial trigeminal neuralgia, and which genes that have been identified in human TN studies and in animal models of trigeminal pain. MedLine, Embase, Cochrane Library and Web of Science were searched from inception to January 2021. 71 studies were included in the systematic review. Currently, few studies provide information about the prevalence of familial TN; the available evidence indicates that about 1–2% of TN cases have the familial form. The available human studies propose the following genes to be possible contributors to development of TN: CACNA1A, CACNA1H, CACNA1F, KCNK1, TRAK1, SCN9A, SCN8A, SCN3A, SCN10A, SCN5A, NTRK1, GABRG1, MPZ gene, MAOA gene and SLC6A4. Their role in familial TN still needs to be addressed. The experimental animal studies suggest an emerging role of genetics in trigeminal pain, though the animal models may be more relevant for trigeminal neuropathic pain than TN per se. In summary, this systematic review suggests a more important role of genetic factors in TN pathogenesis than previously assumed.

Effects of perinatal, late foetal, and early embryonic insults on the cardiovascular phenotype in experimental animal models and humans

VASA ◽  
2016 ◽  
Vol 45 (6) ◽  
pp. 439-449 ◽  
Author(s):  
Theo Arthur Meister ◽  
Emrush Rexhaj ◽  
Stefano Flavio Rimoldi ◽  
Urs Scherrer ◽  
Claudio Sartori
Keyword(s):  
Animal Models ◽  
Experimental Animal ◽  
Genetic Factors ◽  
Assisted Reproductive Technologies ◽  
Disease Risk ◽  
Reproductive Technologies ◽  
Mortality And Morbidity ◽  
Experimental Animal Models ◽  
Experimental Animals ◽  
Underlying Mechanisms

Abstract. Cardiovascular diseases are the main cause of mortality and morbidity in Western countries, but the underlying mechanisms are still poorly understood. Genetic polymorphisms, once thought to represent a major determinant of cardiovascular risk, individually and collectively, only explain a tiny fraction of phenotypic variation and disease risk in humans. It is now clear that non-genetic factors, i.e., factors that modify gene activity without changing the DNA sequence and that are sensitive to the environment can cause important alterations of the cardiovascular phenotype in experimental animal models and humans. Here, we will review recent studies demonstrating that distinct pathological events during the perinatal (transient perinatal hypoxemia), late foetal (preeclampsia), and early embryonic (assisted reproductive technologies) periods induce profound alterations of the cardiovascular phenotype in humans and experimental animals. Moreover, we will provide evidence that epigenetic modifications are contributing importantly to this problem and are conferring the potential for its transmission to subsequent generations.

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