What is he best known for?
The fields of study he is best known for:
Mike Hutton mostly deals with Genetics, Alzheimer's disease, Tau protein, Mutation and Pathology.
His Alzheimer's disease research is multidisciplinary, incorporating elements of Cell biology and Degenerative disease.
His Tau protein research incorporates elements of Progressive supranuclear palsy, Chromosome 17 and Tauopathy.
His Tauopathy research includes elements of Neurofibrillary tangle and Hippocampus, Neuroscience.
Mike Hutton combines subjects such as Frontotemporal lobar degeneration and Exon with his study of Mutation.
His work deals with themes such as Endocrinology and Senile plaques, which intersect with Presenilin.
His most cited work include:
- Association of missense and 5′-splice-site mutations in tau with the inherited dementia FTDP-17 (2839 citations)
- Secreted amyloid β-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease (2304 citations)
- Mutations in progranulin cause tau-negative frontotemporal dementia linked to chromosome 17 (1484 citations)
What are the main themes of his work throughout his whole career to date?
His main research concerns Genetics, Pathology, Tau protein, Frontotemporal dementia and Alzheimer's disease.
The Tau protein study combines topics in areas such as Neurodegeneration, Tauopathy, Molecular biology, Cell biology and Neuroscience.
The study incorporates disciplines such as Neurofibrillary tangle and Transgene in addition to Tauopathy.
His research investigates the connection with Frontotemporal dementia and areas like Parkinsonism which intersect with concerns in Mutation.
His Alzheimer's disease study combines topics in areas such as Apolipoprotein E and Age of onset.
His Presenilin research integrates issues from Pathogenesis and Senile plaques.
He most often published in these fields:
- Genetics (39.60%)
- Pathology (23.83%)
- Tau protein (24.50%)
What were the highlights of his more recent work (between 2007-2017)?
- Neuroscience (17.45%)
- Genetics (39.60%)
- Alzheimer's disease (22.48%)
In recent papers he was focusing on the following fields of study:
Neuroscience, Genetics, Alzheimer's disease, Cell biology and Pathology are his primary areas of study.
The concepts of his Genetics study are interwoven with issues in Dystonia and Parkinsonism.
Mike Hutton has included themes like Gene, Dementia, Immunology and Age of onset in his Alzheimer's disease study.
His Cell biology research includes themes of Caspase, Cleavage, Tau protein and Successful aging.
His studies deal with areas such as Neuronal protein, Kinase and Tauopathy as well as Tau protein.
His research integrates issues of Internal medicine and Genetically modified mouse in his study of Pathology.
Between 2007 and 2017, his most popular works were:
- Wild-Type Human TDP-43 Expression Causes TDP-43 Phosphorylation, Mitochondrial Aggregation, Motor Deficits, and Early Mortality in Transgenic Mice (364 citations)
- Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis. (357 citations)
- Novel mutations in TARDBP (TDP-43) in patients with familial amyotrophic lateral sclerosis. (357 citations)
In his most recent research, the most cited papers focused on:
The scientist’s investigation covers issues in Alzheimer's disease, Frontotemporal lobar degeneration, Mutation, Molecular biology and Frontotemporal dementia.
Mike Hutton studies Tau protein which is a part of Alzheimer's disease.
His Frontotemporal lobar degeneration research is within the category of Pathology.
Mutation is the subject of his research, which falls under Genetics.
He focuses mostly in the field of Molecular biology, narrowing it down to topics relating to TARDBP and, in certain cases, Exon, TAR DNA-Binding Protein 43, Neurodegeneration, Amyotrophic lateral sclerosis and Missense mutation.
His research investigates the connection between Frontotemporal dementia and topics such as Parkinsonism that intersect with issues in Primary progressive aphasia, Atrophy, Chromosome 17 and Tauopathy.
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