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.
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.
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.
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.
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.
Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
David R. Borchelt;Gopal Thinakaran;Christopher B. Eckman;Christopher B. Eckman;Michael K. Lee.
APP processing and synaptic function.
Flavio Kamenetz;Taisuke Tomita;Helen Hsieh;Helen Hsieh;Guy Seabrook.
An adverse property of a familial ALS-linked SOD1 mutation causes motor neuron disease characterized by vacuolar degeneration of mitochondria
Philip C Wong;Carlos A Pardo;David R Borchelt;Michael K Lee.
BACE1 is the major beta-secretase for generation of Abeta peptides by neurons.
Huaibin Cai;Yanshu Wang;Diane McCarthy;Hongjin Wen.
Nature Neuroscience (2001)
Scrapie prion protein contains a phosphatidylinositol glycolipid
Neil Stahl;David R. Borchelt;Karen Hsiao;Stanley B. Prusiner.
ALS-Linked SOD1 Mutant G85R Mediates Damage to Astrocytes and Promotes Rapidly Progressive Disease with SOD1-Containing Inclusions
L. I. Bruijn;M. W. Becher;M. K. Lee;K. L. Anderson.
Accelerated amyloid deposition in the brains of transgenic mice coexpressing mutant presenilin 1 and amyloid precursor proteins
David R Borchelt;Tamara Ratovitski;Judy van Lare;Michael K Lee.
ENDOPROTEOLYSIS OF PRESENILIN 1 AND ACCUMULATION OF PROCESSED DERIVATIVES IN VIVO
Gopal Thinakaran;David R Borchelt;Michael K Lee;Hilda H Slunt.
Mutant presenilins specifically elevate the levels of the 42 residue β-amyloid peptide in vivo: evidence for augmentation of a 42-specific γ secretase
Joanna L. Jankowsky;Joanna L. Jankowsky;Daniel J. Fadale;Jeffrey Anderson;Guilian M. Xu.
Human Molecular Genetics (2004)
Intranuclear Inclusions and Neuritic Aggregates in Transgenic Mice Expressing a Mutant N-Terminal Fragment of Huntingtin
Gabriele Schilling;Mark W. Becher;Alan H. Sharp;Hyder A. Jinnah.
Human Molecular Genetics (1999)
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