نتایج جستجو برای: familial amyotrophic lateral sclerosis fals

تعداد نتایج: 232184  

2017
Alice Vajda Russell L. McLaughlin Mark Heverin Owen Thorpe Sharon Abrahams Ammar Al-Chalabi Orla Hardiman

OBJECTIVE To determine the degree of consensus among clinicians on the clinical use of genetic testing in amyotrophic lateral sclerosis (ALS) and the factors that determine decision-making. METHODS ALS researchers worldwide were invited to participate in a detailed online survey to determine their attitudes and practices relating to genetic testing. RESULTS Responses from 167 clinicians fro...

Journal: :Brain : a journal of neurology 2012
Johnathan Cooper-Knock Christopher Hewitt J Robin Highley Alice Brockington Antonio Milano Somai Man Joanne Martindale Judith Hartley Theresa Walsh Catherine Gelsthorpe Lynne Baxter Gillian Forster Melanie Fox Joanna Bury Kin Mok Christopher J McDermott Bryan J Traynor Janine Kirby Stephen B Wharton Paul G Ince John Hardy Pamela J Shaw

Intronic expansion of the GGGGCC hexanucleotide repeat within the C9ORF72 gene causes frontotemporal dementia and amyotrophic lateral sclerosis/motor neuron disease in both familial and sporadic cases. Initial reports indicate that this variant within the frontotemporal dementia/amyotrophic lateral sclerosis spectrum is associated with transactive response DNA binding protein (TDP-43) proteinop...

2017
Arun Aggarwal

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease which attacks the motor system. Current treatment for sporadic ALS or Cu, Zn superoxide dimutase 1 (SOD 1 mutation) familial ALS, produces only a modest increase in survival. Riluzole, has been available since 1995 and remains the only disease modifying therapy available for ALS. Using the statistical motor unit number est...

Journal: :Human molecular genetics 2011
Lijun Wang David H Gutmann Raymond P Roos

Approximately 10% of patients with amyotrophic lateral sclerosis (ALS) have familial ALS (FALS), and 20% of FALS are caused by mutations of superoxide dismutase type 1 (MTSOD1). The fact that some MTSOD1s that cause FALS have full dismutase activity (e.g. G37R) and others no dismutase activity (e.g. G85R) suggests that MTSOD1 causes FALS due to toxicity of the protein rather than a loss in enzy...

Journal: :Pediatric Neurology Briefs 1998

Journal: :Human molecular genetics 1997
I Kola P J Hertzog

Human chromosome 21 is the smallest human autosome and many important genetic/familial disorders map to this chromosome, e.g., familial amyotrophic lateral sclerosis (FALS), Down syndrome, Alzheimer's disease and some cases of Ewings sarcoma. Hence, the identification of genes localised to this chromosome and studies on their normal biological function and their role in disease is gaining momen...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2007
Arie Gruzman William L Wood Evgenia Alpert M Dharma Prasad Robert G Miller Jeffery D Rothstein Robert Bowser Ronald Hamilton Troy D Wood Don W Cleveland Vishwanath R Lingappa Jian Liu

Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron degenerative disease whose etiology and pathogenesis remain poorly understood. Most cases of ALS ( approximately 90%) are sporadic (SALS), occurring in the absence of genetic associations. Approximately 20% of familial ALS (FALS) cases are due to known mutations in the copper, zinc superoxide dismutase (SOD1) gene. Molecular evid...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2001
A Pramatarova J Laganière J Roussel K Brisebois G A Rouleau

Mutations were identified in the Cu/Zn superoxide dismutase gene (SOD1) in approximately 15% of patients with familial amyotrophic lateral sclerosis. Transgenic animals expressing mutant SOD1 in all tissues develop an ALS-like phenotype. To determine whether neuron-specific expression of mutant SOD1 is sufficient to produce such a phenotype, we generated transgenic animals carrying the G37R mut...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2003
Robin J Mockett Svetlana N Radyuk Judith J Benes William C Orr Rajindar S Sohal

A subset of patients suffering from familial amyotrophic lateral sclerosis (FALS) exhibit point mutations in the gene encoding Cu-Zn superoxide dismutase [superoxide:superoxide oxidoreductase, EC (SOD)]. The human wild-type and five FALS Sod mutant transgenes were introduced into the fruit fly, Drosophila melanogaster, in a Cu-Zn Sod null background. Sod null flies had dramatically decreased li...

Journal: :JAMA neurology 2015
Nimeshan Geevasinga Parvathi Menon James Howells Garth A Nicholson Matthew C Kiernan Steve Vucic

IMPORTANCE Abnormalities of axonal excitability characterized by upregulation of persistent sodium (Na+) conductances and reduced potassium (K+) currents have been reported in sporadic amyotrophic lateral sclerosis (SALS) phenotypes and linked to the development of clinical features such as fasciculations and neurodegeneration. OBJECTIVE To investigate whether abnormalities of axonal ion chan...

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