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Dardiotis E.,University of Thessaly | Dardiotis E.,Institute for Biomedical Technology Biomedical | Grigoriadis S.,Aristotle University of Thessaloniki | Hadjigeorgiou G.M.,University of Thessaly | Hadjigeorgiou G.M.,Institute for Biomedical Technology Biomedical
Current Opinion in Psychiatry | Year: 2012

Purpose of Review: Clinical outcome after neurotrauma is considerably variable and can only partly be explained by known prognostic factors. There is converging evidence from genetic research that a number of genetic variants may contribute to this variability. This review provides recent data from human studies, published in the previous year, on genetic factors influencing outcome after neurotrauma. The bibliographic databases MEDLINE, EMBASE and PsycINFO were searched to identify relevant studies. Recent Findings: Genetic susceptibility to various aspects of clinical outcome after neurotrauma was reported in recent clinical studies. Genetic loci investigated include polymorphisms in APOE, MAO-A, BDNF, NOS3, IL-6, NEFH, SLC6A4, COMT, PPP3CC and KIBRA genes. The importance of these findings and future directions are discussed. Summary: Recent genetic studies have revealed emerging aspects and extended the existing knowledge regarding the pathogenesis of neurotrauma and the genetic influence on phenotypic diversity. A better understanding of the underlying biological pathways and molecular mechanisms of an individual's response to neurotrauma may hold the promise of novel treatment strategies and improved clinical outcome. © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.


Xiromerisiou G.,Institute for Biomedical Technology Biomedical | Dardiotis E.,Institute for Biomedical Technology Biomedical | Dardiotis E.,University Hospital of Larissa | Tsimourtou V.,University Hospital of Larissa | And 6 more authors.
Neurosurgical Focus | Year: 2010

Over the past few years, considerable progress has been made in understanding the molecular mechanisms of Parkinson disease (PD). Mutations in certain genes are found to cause monogenic forms of the disorder, with autosomal dominant or autosomal recessive inheritance. These genes include alpha-synuclein, parkin, PINK1, DJ-1, LRRK2, and ATP13A2. The monogenic variants are important tools in identifying cellular pathways that shed light on the pathogenesis of this disease. Certain common genetic variants are also likely to modulate the risk of PD. International collaborative studies and meta-analyses have identified common variants as genetic susceptibility risk/protective factors for sporadic PD.


PubMed | Institute for Biomedical Technology Biomedical
Type: Journal Article | Journal: Neurosurgical focus | Year: 2010

Over the past few years, considerable progress has been made in understanding the molecular mechanisms of Parkinson disease (PD). Mutations in certain genes are found to cause monogenic forms of the disorder, with autosomal dominant or autosomal recessive inheritance. These genes include alpha-synuclein, parkin, PINK1, DJ-1, LRRK2, and ATP13A2. The monogenic variants are important tools in identifying cellular pathways that shed light on the pathogenesis of this disease. Certain common genetic variants are also likely to modulate the risk of PD. International collaborative studies and meta-analyses have identified common variants as genetic susceptibility risk/protective factors for sporadic PD.

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