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Claudia F. Lucchinetti, M viagra online .D., Bogdan F.G. Popescu, M.D., Ph.D., Reem F. Bunyan, M.D., Natalia M. Moll, M.D., Ph.D., Shanu F. Roemer, M.D., Hans Lassmann, M.D.D., Joseph E. Parisi, M.D., Bernd W. Scheithauer, M.D., Caterina Giannini, M.D., Stephen D. Weigand, M.S., Jay Mandrekar, Ph.D., and Richard M. Ransohoff, M.D.: Inflammatory Cortical Demyelination in Early Multiple Sclerosis Diagnostic, therapeutic, and investigative attempts in multiple sclerosis have concentrated in disease of the white matter. Imaging and histopathological studies claim that cortical damage can be a correlate of cognitive disease and dysfunction progression, reflecting demyelination or secondary neurodegeneration.1-7 Three types of cortical plaques have been described: leukocortical lesions, which extend from the white matter in to the cortex; intracortical lesions, which project from microvessels radially; and subpial lesions, which extend from the pia mater intracortically.5,8 Subpial, bandlike, demyelinated plaques involve contiguous gyri often, 6 favoring those parts of the brain involved in attention and memory processing.6,8,9 Studies of postmortem cells from patients with long-standing multiple sclerosis have resulted in the suggestion that cortical demyelination contributes to disability in patients with progressive multiple sclerosis,6 occurs of white-matter lesions independently,6 is driven by organized meningeal inflammatory infiltrates10,11 and is devoid of parenchymal macrophages and lymphocytes,4,5,8 suggesting that neurodegeneration proceeds independently of parenchymal inflammation.

These self-complementary AAV vectors mediate transgene expression at substantially higher levels than do single-stranded AAV vectors.6,10 Second, to circumvent the possibility of humoral immunity to AAV, we pseudotyped these vectors with a capsid of serotype 8 , that includes a lower seroprevalence in humans than does AAV2.6,7,10 Methods Research Design Patients who also met the entry criteria and did not have neutralizing antibodies to AAV8, as determined by an in vivo transduction-inhibition assay , were enrolled after providing written informed consent. Participants 1 through 5 were recruited this year 2010 and Participant 6 was recruited early in 2011. All were admitted to the Royal Totally free Medical center for vector administration and subsequent observation overnight.