نتایج جستجو برای: survival motor neuron gene

تعداد نتایج: 1595196  

Journal: :Journal of Neuropathology and Experimental Neurology 2006

Journal: :iranian journal of public health 0
h aryan o aryani k banihashemi t zaman m houshmand

background: sandhoff disease is an autosomal recessive disorder caused by β-hexosaminidase deficiency and accumulation of gm2 ganglioside resulting in progressive motor neuron manifestations and death from respiratory failure and infections in infantiles. pathogenic mutations in hexb gene were observed which leads to enzyme activity reduction and interruption of normal metabolic cycle of gm2 ga...

Journal: :Mechanisms of Development 2005
Jennifer Whitehead Cynthia Keller-Peck Jan Kucera Warren G. Tourtellotte

Glial cell-line derived neurotrophic factor (GDNF) is a potent survival factor for motor neurons. Previous studies have shown that some motor neurons depend upon GDNF during development but this GDNF-dependent motor neuron subpopulation has not been characterized. We examined GDNF expression patterns in muscle and the impact of altered GDNF expression on the development of subtypes of motor neu...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2012
Tara L Martinez Lingling Kong Xueyong Wang Melissa A Osborne Melissa E Crowder James P Van Meerbeke Xixi Xu Crystal Davis Joe Wooley David J Goldhamer Cathleen M Lutz Mark M Rich Charlotte J Sumner

The inherited motor neuron disease spinal muscular atrophy (SMA) is caused by deficient expression of survival motor neuron (SMN) protein and results in severe muscle weakness. In SMA mice, synaptic dysfunction of both neuromuscular junctions (NMJs) and central sensorimotor synapses precedes motor neuron cell death. To address whether this synaptic dysfunction is due to SMN deficiency in motor ...

2014
Lucio Tremolizzo Gessica Sala Elisa Conti Virginia Rodriguez-Menendez Antonella Fogli Angela Michelucci Paolo Simi Silvana Penco Christian Lunetta Massimo Corbo Carlo Ferrarese

Here we report the case of an ALS patient found to carry both a novel heterozygous change (c.194G>A) within the spastin gene and a homozygous deletion of the SMN2 gene. The patient was started on valproic acid (VPA, 600 mg/die per os) considering the capacity of this drug of increasing survival motor neuron through an epigenetic mechanism. Patient clinical course and molecular effects of VPA on...

Journal: :Genes & development 2010
Arthur H M Burghes Vicki L McGovern

Antisense oligonucleotides (ASOs) can be used to alter the splicing of a gene and either restore production of a required protein or eliminate a toxic product. In this issue of Genes & Development, Hua and colleagues (pp. 1634-1644) show that ASOs directed against an intron splice silencer (ISS) in the survival motor neuron 2 (SMN2) gene alter the amount of full-length SMN transcript in the ner...

Journal: :Arquivos de neuro-psiquiatria 2016
Paulo Victor Sgobbi de Souza Wladimir Bocca Vieira de Rezende Pinto Flávio Moura Rezende Acary Souza Bulle Oliveira

Motor neuron disease is one of the major groups of neurodegenerative diseases, mainly represented by amyotrophic lateral sclerosis. Despite wide genetic and biochemical data regarding its pathophysiological mechanisms, motor neuron disease develops under a complex network of mechanisms not restricted to the unique functions of the alpha motor neurons but which actually involve diverse functions...

Journal: :journal of rehabilitation sciences and research 0
amin yoosefi kordi assistant professor, department of physiotherapy, school of rehabilitation sciences, shiraz university of medical sciences, shiraz, iran. fatemeh jabari department of physiotherapy, school of rehabilitation sciences, shiraz university of medical sciences, shiraz, iran. mahnaz setooni department of physiotherapy, school of rehabilitation sciences, shiraz university of medical sciences, shiraz, iran.

background: als is the most devastating form of motor neuron disease, and the chance of survival is 3 to 5 years after the diagnosis is made. the pathogenesis of the disease is unknown. several upper and lower motor neuron symptoms such as weakness, gait bradykinesia, and muscle atrophy have been reported. the core muscles are considered to be the center of the functional kinetic chain due to t...

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