Institute for Biomedical Technology Biomedical

Greece

Institute for Biomedical Technology Biomedical

Greece
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Dardiotis E.,The Cyprus Institute of Neurology and Genetics | Panayiotou E.,The Cyprus Institute of Neurology and Genetics | Feldman M.L.,The Cyprus Institute of Neurology and Genetics | Hadjisavvas A.,The Cyprus Institute of Neurology and Genetics | And 5 more authors.
Neuroscience Letters | Year: 2013

In amyotrophic lateral sclerosis (ALS) reactive oxygen species and apoptosis are implicated in disease pathogenesis. Melatonin with its anti-oxidant and anti-apoptotic properties is expected to ameliorate disease phenotype. The aim of this study was to assess possible neuroprotection of melatonin in the G93A-copper/zinc superoxide dismutase (G93ASOD1) transgenic mouse model of ALS. Four groups of mice, 14 animals each, were injected intraperitoneally with 0. mg/kg, 0.5. mg/kg, 2.5. mg/kg and 50. mg/kg of melatonin from age 40 days. The primary end points were; disease onset, disease duration, survival and rotarod performance. No statistically significant difference in disease onset between the four groups was found. Survival was significantly reduced with the 0.5. mg/kg and 50. mg/kg doses and tended to be reduced with the 2.5. mg/kg dose. Histological analysis of spinal cords revealed increased motoneuron loss in melatonin treated mice. Melatonin treated animals were associated with increased oxidative stress as assessed with 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation. Histochemistry and Western blot data of spinal cord from melatonin treated mice revealed upregulation of human SOD1 compared to untreated mice. In addition, real-time PCR revealed a dose dependent upregulation of human SOD1 in melatonin treated animals. Thus, intraperitoneal melatonin, at the doses used, does not ameliorate and perhaps exacerbates phenotype in the G93ASOD1 mouse ALS model. This is probably due to melatonin's effect on upregulating gene expression of human toxic SOD1. This action presumably overrides any of its direct anti-oxidant and anti-apoptotic properties. © 2013 Elsevier Ireland Ltd.


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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