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  The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease

Zhai, J., Zhou, W., Li, J., Hayworth, C. R., Zhang, L., Misawa, H., et al. (2011). The in vivo contribution of motor neuron TrkB receptors to mutant SOD1 motor neuron disease. Human Molecular Genetics, 20(21), 4116-4131. doi:10.1093/hmg/ddr335.

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 Urheber:
Zhai, Jinbin, Autor
Zhou, Weiguo, Autor
Li, Jian, Autor
Hayworth, Christopher R., Autor
Zhang, Lei, Autor
Misawa, Hidemi, Autor
Klein, Rüdiger1, Autor           
Scherer, Steven S., Autor
Balice-Gordon, Rita J., Autor
Kalb, Robert Gordon, Autor
Affiliations:
1Department: Molecular Neurobiology / Klein, MPI of Neurobiology, Max Planck Society, ou_1113546              

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Schlagwörter: AMYOTROPHIC-LATERAL-SCLEROSIS; CULTURED CORTICAL-NEURONS; NEUROTROPHIC FACTOR; MELANOCORTIN-4 RECEPTOR; SPINAL MOTONEURONS; DENDRITIC GROWTH; TRANSGENIC MICE; ENERGY-BALANCE; NADPH OXIDASE; BRAINBiochemistry & Molecular Biology; Genetics & Heredity;
 Zusammenfassung: Brain-derived neurotrophic factor (BDNF) and its receptor
tropomyosin-related kinase B (TrkB) are widely expressed in the
vertebrate nervous system and play a central role in mature neuronal
function. In vitro BDNF/TrkB signaling promotes neuronal survival and
can help neurons resist toxic insults. Paradoxically, BDNF/TrkB
signaling has also been shown, under certain in vitro circumstances, to
render neurons vulnerable to insults. We show here that in vivo
conditional deletion of TrkB from mature motor neurons attenuates
mutant superoxide dismutase 1 (SOD1) toxicity. Mutant SOD1 mice lacking
motor neuron TrkB live a month longer than controls and retain motor
function for a longer period, particularly in the early phase of the
disease. These effects are subserved by slowed motor neuron loss,
persistence of neuromuscular junction integrity and reduced astrocytic
and microglial reactivity within the spinal cord. These results suggest
that manipulation of BDNF/TrkB signaling might have therapeutic
efficacy in motor neuron diseases.

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Sprache(n): eng - English
 Datum: 2011
 Publikationsstatus: Erschienen
 Seiten: 16
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000295686000003
DOI: 10.1093/hmg/ddr335
 Art des Abschluß: -

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Titel: Human Molecular Genetics
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: Oxford, England : IRL Press
Seiten: - Band / Heft: 20 (21) Artikelnummer: - Start- / Endseite: 4116 - 4131 Identifikator: ISSN: 0964-6906
CoNE: https://pure.mpg.de/cone/journals/resource/954925581153