What is he best known for?
The fields of study he is best known for:
Molecular biology, Genetically modified mouse, Transgene, Neuroscience and Amyloid precursor protein are his primary areas of study.
His Molecular biology research includes themes of Scrapie, Protease and Gene.
His research integrates issues of Huntington's disease and Mutant in his study of Genetically modified mouse.
His Mutant research is multidisciplinary, incorporating elements of Motor neuron and Superoxide dismutase.
His study in Neuroscience is interdisciplinary in nature, drawing from both Disease, Amyloid precursor protein secretase and Amyloidosis.
His Amyloid precursor protein research integrates issues from Presenilin and Senile plaques.
His most cited work include:
- Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo (1356 citations)
- APP processing and synaptic function. (1315 citations)
- An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria (1271 citations)
What are the main themes of his work throughout his whole career to date?
The scientist’s investigation covers issues in Genetically modified mouse, Molecular biology, Transgene, Mutant and SOD1.
His Genetically modified mouse research includes elements of Amyloid precursor protein, Pathology, Cell biology, Huntingtin and Neuroscience.
He has researched Amyloid precursor protein in several fields, including Presenilin and Amyloid.
His work deals with themes such as RNA and Gene, which intersect with Molecular biology.
His research on Transgene often connects related topics like Pathogenesis.
His studies deal with areas such as Mutation and Mutant protein as well as SOD1.
He most often published in these fields:
- Genetically modified mouse (46.60%)
- Molecular biology (26.53%)
- Transgene (27.55%)
What were the highlights of his more recent work (between 2013-2021)?
- Genetically modified mouse (46.60%)
- Amyotrophic lateral sclerosis (22.11%)
- Cell biology (22.79%)
In recent papers he was focusing on the following fields of study:
David R. Borchelt mainly focuses on Genetically modified mouse, Amyotrophic lateral sclerosis, Cell biology, SOD1 and Pathology.
His Genetically modified mouse research is within the category of Transgene.
His Transgene study which covers Amyloid that intersects with Alzheimer's disease.
His Amyotrophic lateral sclerosis study incorporates themes from Phenotype, Neurodegeneration and Motor neuron, Neuroscience, Spinal cord.
The Cell biology study which covers Peripheral myelin protein 22 that intersects with Lipid droplet and Lipid raft.
His work carried out in the field of SOD1 brings together such families of science as Mutation, Molecular biology and Yellow fluorescent protein.
Between 2013 and 2021, his most popular works were:
- Intramuscular injection of α-synuclein induces CNS α-synuclein pathology and a rapid-onset motor phenotype in transgenic mice (196 citations)
- C9orf72 BAC Mouse Model with Motor Deficits and Neurodegenerative Features of ALS/FTD (184 citations)
- RAN Translation in Huntington Disease (172 citations)
In his most recent research, the most cited papers focused on:
His primary areas of study are Genetically modified mouse, Pathology, Amyotrophic lateral sclerosis, Transgene and Mutation.
His studies examine the connections between Genetically modified mouse and genetics, as well as such issues in Amyloidosis, with regards to Water maze, Behavioral test, Presenilin, Amyloid precursor protein and P3 peptide.
His studies in Amyotrophic lateral sclerosis integrate themes in fields like Superoxide dismutase, Motor neuron and Frontotemporal dementia.
His Transgene study combines topics in areas such as Neurodegeneration, Protein aggregation and Amyloid.
The Mutation study combines topics in areas such as Protein structure, Molecular biology, Nuclear localization sequence and RNA-binding protein.
His Molecular biology research is multidisciplinary, relying on both Mutant and SOD1.
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