Kleopas A Kleopa


Affiliation: The Cyprus Institute of Neurology and Genetics
Country: Cyprus


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    Kleopa K, Zamba Papanicolaou E, Alevra X, Nicolaou P, Georgiou D, Hadjisavvas A, et al. Phenotypic and cellular expression of two novel connexin32 mutations causing CMT1X. Neurology. 2006;66:396-402 pubmed
    ..The position and cellular expression of Cx32 mutations alone cannot fully predict these phenotypic variations in CMT1X. ..
  2. Kagiava A, Kleopa K. Intrathecal Delivery of Viral Vectors for Gene Therapy. Methods Mol Biol. 2018;1791:277-285 pubmed publisher
    ..This gene delivery route provides widespread and stable over time Schwann cell-targeted or ubiquitous gene expression in the peripheral nervous system. ..
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    Kleopa K, Orthmann Murphy J, Sargiannidou I. Gap junction disorders of myelinating cells. Rev Neurosci. 2010;21:397-419 pubmed
    ..Here we review the clinical, genetic, and neurobiological aspects of GJ disorders affecting the PNS and CNS myelinating cells. ..
  4. Kagiava A, Theophilidis G, Sargiannidou I, Kyriacou K, Kleopa K. Oxaliplatin-induced neurotoxicity is mediated through gap junction channels and hemichannels and can be prevented by octanol. Neuropharmacology. 2015;97:289-305 pubmed publisher
    ..The GJ blocker octanol prevents OIN at very low concentrations and should be further studied as a neuroprotectant. ..
  5. Kleopa K, Sargiannidou I. Connexins, gap junctions and peripheral neuropathy. Neurosci Lett. 2015;596:27-32 pubmed publisher
    ..Increased understanding of CMT1X pathogenesis will lead to the development of effective therapies for this currently incurable disease. ..
  6. Olympiou M, Sargiannidou I, Markoullis K, Karaiskos C, Kagiava A, Kyriakoudi S, et al. Systemic inflammation disrupts oligodendrocyte gap junctions and induces ER stress in a model of CNS manifestations of X-linked Charcot-Marie-Tooth disease. Acta Neuropathol Commun. 2016;4:95 pubmed publisher
    ..Moreover the presence of an intracellularly retained, misfolded CMT1X mutant such as T55I induces ER stress under inflammatory conditions, further exacerbating oligodendrocyte dysfunction and pathological changes in the CNS. ..
  7. Konstantopoulos K, Christou Y, Vogazianos P, Zamba Papanicolaou E, Kleopa K. A quantitative method for the assessment of dysarthrophonia in myasthenia gravis. J Neurol Sci. 2017;377:42-46 pubmed publisher
    ..This study demonstrates that non-invasive physiological methods (EGG and speech acoustics) offer essential tools for the assessment of dysarthrophonia in MG patients. ..
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    Kleopa K, Orthmann J, Enriquez A, Paul D, Scherer S. Unique distributions of the gap junction proteins connexin29, connexin32, and connexin47 in oligodendrocytes. Glia. 2004;47:346-57 pubmed
    ..This diversity of connexins in oligodendrocytes (in different populations of cells and in different subcellular compartments) likely reflects functional differences between these connexins and perhaps the oligodendrocytes themselves. ..
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    Kleopa K, Elman L, Lang B, Vincent A, Scherer S. Neuromyotonia and limbic encephalitis sera target mature Shaker-type K+ channels: subunit specificity correlates with clinical manifestations. Brain. 2006;129:1570-84 pubmed
    ..Although more than one type of antibody is often detectable in individual sera, higher affinity for certain subunits or subunit combinations may determine the range of clinical manifestations...

More Information


  1. Schiza N, Sargiannidou I, Kagiava A, Karaiskos C, Nearchou M, Kleopa K. Transgenic replacement of Cx32 in gap junction-deficient oligodendrocytes rescues the phenotype of a hypomyelinating leukodystrophy model. Hum Mol Genet. 2015;24:2049-64 pubmed publisher
    ..Our study confirms that loss of oligodendrocyte GJs has cell autonomous effects and that re-establishment of GJ connectivity by replacement of least one GJ protein provides correction of the leukodystrophy phenotype. ..