Carsten Wessig

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The integrity of peripheral nerves relies on communication between axons and Schwann cells. The axonal signals that ensure myelin maintenance are distinct from those that direct myelination and are largely unknown. Here we show that ablation of the prion protein PrP(C) triggers a chronic demyelinating polyneuropathy (CDP) in four independently targeted(More)
Late-onset glycogen storage disease type 2 (GSD2)/Pompe disease is a progressive multi-system disease evoked by a deficiency of lysosomal acid α-glucosidase (GAA) activity. GSD2 is characterized by respiratory and skeletal muscle weakness and atrophy, resulting in functional disability and reduced life span. Since 2006 alglucosidase alfa has been licensed(More)
Using newly generated transgenic mice in which the coding region of the connexin29 (Cx29) gene was replaced by the lacZ reporter gene, we confirmed previous immunochemical results that Cx29 is expressed in Schwann cells, oligodendrocytes and Bergmann glia cells. In addition, we detected lacZ/Cx29 in Schwann cells of the sciatic nerve and in particular of(More)
OBJECTIVES Recently, we proposed a new stimulation paradigm for brain computer interfaces (BCI) based on event-related potentials (ERP), i.e. flashing characters with superimposed pictures of well-known faces. This new face flashing (FF) paradigm significantly outperformed the commonly used character flashing (CF) approach, i.e. simply highlighting(More)
BACKGROUND AND PURPOSE MR changes in denervated muscles have been reported to occur within days up to several weeks after peripheral nerve damage. The purpose of this experimental study was to investigate the longitudinal changes in denervated muscles by using MR imaging. METHODS In 12 Lewis rats, the left sciatic nerve was transected at the level of the(More)
A deficiency of arylsulfatase A (ASA) causes the lysosomal storage disease metachromatic leukodystrophy, which is characterized by accumulation of the sphingolipid 3-O-sulfogalactosylceramide (sulfatide). Sphingolipid storage results in progressive demyelination and severe neurologic symptoms. The disease is lethal, and curative therapy is not available. To(More)
Mice heterozygously deficient for myelin protein zero (P0) mimicking human Charcot-Marie-Tooth (CMT) disease 1B show T-lymphocyte and macrophage upregulation in peripheral nerves, which aggravates and modulates the genetically mediated demyelinating neuropathy. In connexin32 (cx32)-deficient (cx32(def)) mice, which mimic the X-linked dominant form of CMT(More)
Mice deficient in the peripheral myelin component P0 mimic severe forms of inherited peripheral neuropathies in humans, with defective myelin formation and consequent axonal loss. We cross-bred these mice with the spontaneous mutant C57BL/Wld(s) typically showing protection from Wallerian degeneration because of fusion of the ubiquitination factor E4B(More)
Magnetic resonance imaging (MRI) is a powerful tool to assess brain lesions, but currently available contrast agents are limited in the assessment of cellular and functional alterations. By use of the novel MRI contrast agent gadofluorine M (Gf) we report on imaging of transient and widespread changes of blood-brain barrier (BBB) properties as a consequence(More)
Amyotrophic lateral sclerosis (ALS), the major form of motor neuron disease in the adult occurs as a sporadic disease in more than 95% of all cases. Analysis of familial forms is considered as a key to understand the pathophysiology of the disease. It is expected that mutations responsible for familial forms are also found in sporadic ALS. During the past(More)