@article{LueningschroerBinottiDombertetal.2017,
  author    = {L{\"u}ningschr{\"o}r, Patrick and Binotti, Beyenech and Dombert, Benjamin and Heimann, Peter and Perez-Lara, Angel and Slotta, Carsten and Thau-Habermann, Nadine and von Collenberg, Cora R. and Karl, Franziska and Damme, Markus and Horowitz, Arie and Maystadt, Isabelle and F{\"u}chtbauer, Annette and F{\"u}chtbauer, Ernst-Martin and Jablonka, Sibylle and Blum, Robert and {\"U}{\c{c}}eyler, Nurcan and Petri, Susanne and Kaltschmidt, Barbara and Jahn, Reinhard and Kaltschmidt, Christian and Sendtner, Michael},
  title     = {Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease},
  series = {Nature Communications},
  volume    = {8},
  journal   = {Nature Communications},
  number    = {678},
  doi       = {10.1038/s41467-017-00689-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-170048},
  year      = {2017},
  abstract  = {Autophagy-mediated degradation of synaptic components maintains synaptic homeostasis but also constitutes a mechanism of neurodegeneration. It is unclear how autophagy of synaptic vesicles and components of presynaptic active zones is regulated. Here, we show that Pleckstrin homology containing family member 5 (Plekhg5) modulates autophagy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to preautophagosomal structures. Plekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axon terminals. Plekhg5-depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutively active Rab26. These findings define a mechanism for regulating autophagy in neurons that specifically targets synaptic vesicles. Disruption of this mechanism may contribute to the pathophysiology of several forms of motoneuron disease.},
  language  = {en}
}
@article{UeceylerSchaeferMackenrodtetal.2016,
  author    = {{\"U}{\c{c}}eyler, Nurcan and Sch{\"a}fer, Kristina A. and Mackenrodt, Daniel and Sommer, Claudia and M{\"u}llges, Wolfgang},
  title     = {High-Resolution Ultrasonography of the Superficial Peroneal Motor and Sural Sensory Nerves May Be a Non-invasive Approach to the Diagnosis of Vasculitic Neuropathy},
  series = {Frontiers in Neurology},
  volume    = {7},
  journal   = {Frontiers in Neurology},
  number    = {48},
  doi       = {10.3389/fneur.2016.00048},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-146671},
  year      = {2016},
  abstract  = {High-resolution ultrasonography (HRUS) is an emerging new tool in the investigation of peripheral nerves. We set out to assess the utility of HRUS performed at lower extremity nerves in peripheral neuropathies. Nerves of 26 patients with polyneuropathies of different etiologies and 26 controls were investigated using HRUS. Patients underwent clinical, laboratory, electrophysiological assessment, and a diagnostic sural nerve biopsy as part of the routine work-up. HRUS was performed at the sural, tibial, and the common, superficial, and deep peroneal nerves. The superficial peroneal nerve longitudinal diameter (LD) distinguished best between the groups: patients with immune-mediated neuropathies (n = 13, including six with histology-proven vasculitic neuropathy) had larger LD compared to patients with non-immune-mediated neuropathies (p < 0.05) and to controls (p < 0.001). Among all subgroups, patients with vasculitic neuropathy showed the largest superficial peroneal nerve LD (p < 0.001) and had a larger sural nerve cross-sectional area when compared with disease controls (p < 0.001). Enlargement of the superficial peroneal and sural nerves as detected by HRUS may be a useful additional finding in the differential diagnosis of vasculitic and other immune-mediated neuropathies.},
  language  = {en}
}