Garth A. Nicholson mostly deals with Genetics, Amyotrophic lateral sclerosis, Mutation, Gene and Missense mutation. Garth A. Nicholson has included themes like C9orf72, Frontotemporal dementia, Genome-wide association study and RNA-Binding Protein FUS in his Amyotrophic lateral sclerosis study. His work deals with themes such as C9orf72 Protein and TARDBP, which intersect with C9orf72.
He works mostly in the field of TARDBP, limiting it down to topics relating to TAR DNA-Binding Protein 43 and, in certain cases, Neurodegeneration. The Mutation study combines topics in areas such as Molecular biology and Glycine—tRNA ligase. His work in Gene addresses issues such as DNA, which are connected to fields such as RNA and Juvenile amyotrophic lateral sclerosis.
The scientist’s investigation covers issues in Genetics, Gene, Amyotrophic lateral sclerosis, Mutation and Pathology. All of his Genetics and Locus, Genetic linkage, Haplotype, Exome sequencing and Missense mutation investigations are sub-components of the entire Genetics study. The concepts of his Locus study are interwoven with issues in X chromosome and Gene mapping.
His Genetic linkage research integrates issues from Genetic marker, Chromosome, Linkage and Neuroscience. His Gene research is multidisciplinary, relying on both Molecular biology and Disease. He combines subjects such as C9orf72, Frontotemporal dementia and Genome-wide association study with his study of Amyotrophic lateral sclerosis.
Genetics, Amyotrophic lateral sclerosis, Gene, Mutation and Exome sequencing are his primary areas of study. His study in Disease extends to Genetics with its themes. His Amyotrophic lateral sclerosis study integrates concerns from other disciplines, such as Missense mutation, Genome-wide association study, DNA methylation and C9orf72.
His C9orf72 research is multidisciplinary, relying on both Asymptomatic and Outpatient clinic. In his research on the topic of Mutation, Soma and Downregulation and upregulation is strongly related with Pathogenesis. His Exome sequencing research is multidisciplinary, incorporating elements of Age of onset, Compound heterozygosity and Myopathy.
His scientific interests lie mostly in Genetics, Amyotrophic lateral sclerosis, Exome sequencing, Exome and Mutation. His studies in Gene, Locus, Phenotype and Hereditary spastic paraplegia are all subfields of Genetics research. The study incorporates disciplines such as Missense mutation, Genome-wide association study, Case-control study and Gene mutation in addition to Amyotrophic lateral sclerosis.
In his study, C9orf72 is inextricably linked to TARDBP, which falls within the broad field of Gene mutation. The Exome study combines topics in areas such as Metabolic myopathy and Bethlem myopathy. His research integrates issues of Arginine, Ornithine and Candidate gene in his study of Mutation.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
TDP-43 Mutations in Familial and Sporadic Amyotrophic Lateral Sclerosis
Jemeen Sreedharan;Ian P. Blair;Vineeta B. Tripathi;Xun Hu.
Science (2008)
Mutations in FUS, an RNA Processing Protein, Cause Familial Amyotrophic Lateral Sclerosis Type 6
Caroline Vance;Boris Rogelj;Tibor Hortobágyi;Kurt J. De Vos.
Science (2009)
DNA/RNA Helicase Gene Mutations in a Form of Juvenile Amyotrophic Lateral Sclerosis (ALS4)
Ying Zhang Chen;Craig L. Bennett;Huy M. Huynh;Ian P. Blair.
American Journal of Human Genetics (2004)
Controversies and priorities in amyotrophic lateral sclerosis
Martin R Turner;Orla Hardiman;Michael Benatar;Benjamin R Brooks.
Lancet Neurology (2013)
Mutations in SPTLC1 , encoding serine palmitoyltransferase, long chain base subunit-1, cause hereditary sensory neuropathy type I
Jennifer L. Dawkins;Dennis J. Hulme;Sonal B. Brahmbhatt;Michaela Auer-Grumbach.
Nature Genetics (2001)
Cortical hyperexcitability may precede the onset of familial amyotrophic lateral sclerosis
Steve Vucic;Garth A. Nicholson;Matthew C. Kiernan.
Brain (2008)
Mutations in the pleckstrin homology domain of dynamin 2 cause dominant intermediate Charcot-Marie-Tooth disease
Stephan Züchner;Stephan Züchner;Maher Noureddine;Marina Kennerson;Kristien Verhoeven.
Nature Genetics (2005)
A yeast functional screen predicts new candidate ALS disease genes
Julien Couthouis;Michael P. Hart;James Shorter;Mariely DeJesus-Hernandez.
Proceedings of the National Academy of Sciences of the United States of America (2011)
The peripheral myelin gene PMP-22/GAS-3 is duplicated in Charcot-Marie-Tooth disease type 1A.
L. J. Valentijn;P. A. Bolhuis;I. Zorn;J. E. Hoogendijk.
Nature Genetics (1992)
Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis
Wouter van Rheenen;Aleksey Shatunov;Annelot M. Dekker;Russell L. McLaughlin.
Nature Genetics (2016)
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