Journal of Stroke & Cerebrovascular Diseases
Volume 18, Issue 5 , Pages 360-362 , September 2009

Evaluation of the Genetic Variants of Kinesin Motor Protein in Ischemic Stroke

  • Zoltan Szolnoki, MD, PhD

      Affiliations

    • Department of Cerebrovascular Diseases, Pándy Kálmán County Hospital, Gyula, Hungary
    • Corresponding Author InformationAddress correspondence to Zoltan Szolnoki, MD, PhD, H-5600 Békéscsaba, Pipacs köz 9, Hungary.
    • ,
  • Julianna Serly, BSc

      Affiliations

    • Department of Medical Microbiology and Immunology, Faculty of Medicine, University of Szeged, Hungary
    • ,
  • Andras Kondacs, BSc

      Affiliations

    • Department of Cerebrovascular Diseases, Pándy Kálmán County Hospital, Gyula, Hungary
    • ,
  • Yvette Mandi, MD, PhD, DSc

      Affiliations

    • Department of Medical Microbiology and Immunology, Faculty of Medicine, University of Szeged, Hungary
    • ,
  • Ferenc Somogyvari, BSc, PhD

      Affiliations

    • Department of Medical Microbiology and Immunology, Faculty of Medicine, University of Szeged, Hungary

Received 20 November 2008 ,Revised 31 December 2008 ,Accepted 6 January 2009.

References 

  1. Szolnoki Z, Melegh B. Gene-gene and gene-environment interplay represent specific susceptibility for different types of ischemic stroke and leukoaraiosis. Curr Med Chem. 2006;13:1627–1634
  2. Basile AM, Pantoni L, Pracucci G, et al. LADIS Study Group Age, hypertension, and lacunar stroke are the major determinants of the severity of age-related white matter changes: The LADIS (leukoaraiosis and disability in the elderly) study. Cerebrovasc Dis. 2006;2:315–322
  3. Khan U, Porteous L, Hassan A, et al. Risk factor profile of cerebral small vessel disease and its subtypes. J Neurol Neurosurg Psychiatry. 2007;78:702–706
  4. Hachinski VC, Potter P, Merskey H. Leuko-araiosis: An ancient term for a new problem. Can J Neurol Sci. 1986;13:533–534
  5. Szolnoki Z. Pathomechanism of leukoaraiosis: A molecular bridge between the genetic, biochemical, and clinical processes (a mitochondrial hypothesis). Neuromol Med. 2007;9:21–33
  6. Szolnoki Z, Kondacs A, Mandi Y, et al. Evaluation of the roles of the A185C and C406T kinesin light-chain 1 variants in the development of leukoaraiosis. Neurosci Lett. 2007;429:101–104
  7. Szolnoki Z, Kondacs A, Mandi Y, et al. A genetic variant in cytoskeleton motors amplifies susceptibility to leukoaraiosis in hypertensive smokers: Gene-environmental interactions behind vascular white matter demyelinization. J Mol Neurosci. 2007;33:173–179
  8. Abe K, Aoki M, Kawagoe J, et al. Ischemic delayed neuronal death: A mitochondrial hypothesis. Stroke. 1995;26:1478–1489
  9. Szolnoki Z, Somogyvári F, Kondacs A, et al. Evaluation of the interactions of common genetic mutations in stroke subtypes. J Neurol. 2002;249:1391–1397
  10. Szolnoki Z. Chemical events behind leukoaraiosis: Medicinal chemistry offers a new insight into a specific microcirculation disturbance in the brain (a chemical approach to a frequent cerebral phenotype). Curr Med Chem. 2007;14:1027–1036
  11. Markus HS, Lythgoe DJ, Ostegaard L, et al. Reduced cerebral blood flow in white matter in ischemic leukoaraiosis demonstrated using quantitative exogenous contrast based perfusion MRI. J Neurol Neurosurg Psychiatry. 2000;69:48–53
  12. Markus HS. Genes, endothelial function and cerebral small vessel disease in man. Exp Physiol. 2008;93:121–127
  13. Pantoni L. Pathophysiology of age-related cerebral white matter changes. Cerebrovasc Dis. 2002;13:7–14

PII: S1052-3057(09)00019-6

doi: 10.1016/j.jstrokecerebrovasdis.2009.01.004

Journal of Stroke & Cerebrovascular Diseases
Volume 18, Issue 5 , Pages 360-362 , September 2009

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