H-Index & Metrics Best Publications

H-Index & Metrics

Discipline name H-index Citations Publications World Ranking National Ranking
Biology and Biochemistry D-index 77 Citations 34,550 181 World Ranking 2025 National Ranking 1133

Overview

What is he best known for?

The fields of study he is best known for:

  • Gene
  • Enzyme
  • DNA

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:

  • Gene
  • Enzyme
  • DNA

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.

Best Publications

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.
Neuron (1996)

1833 Citations

APP processing and synaptic function.

Flavio Kamenetz;Taisuke Tomita;Helen Hsieh;Helen Hsieh;Guy Seabrook.
Neuron (2003)

1792 Citations

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.
Neuron (1995)

1582 Citations

BACE1 is the major beta-secretase for generation of Abeta peptides by neurons.

Huaibin Cai;Yanshu Wang;Diane McCarthy;Hongjin Wen.
Nature Neuroscience (2001)

1487 Citations

Scrapie prion protein contains a phosphatidylinositol glycolipid

Neil Stahl;David R. Borchelt;Karen Hsiao;Stanley B. Prusiner.
Cell (1987)

1482 Citations

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.
Neuron (1997)

1416 Citations

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.
Neuron (1997)

1410 Citations

ENDOPROTEOLYSIS OF PRESENILIN 1 AND ACCUMULATION OF PROCESSED DERIVATIVES IN VIVO

Gopal Thinakaran;David R Borchelt;Michael K Lee;Hilda H Slunt.
Neuron (1996)

1245 Citations

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)

1201 Citations

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)

996 Citations

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