Robert H. Brown
Impact in
Papers in
- Co-authors
- Eric Hoffman (8 shared papers)Louis M. Kunkel (4 shared papers)Piera Pasinelli (16 shared papers)Ammar Al‐Chalabi (17 shared papers)Don W. Cleveland (7 shared papers)J. Paul Taylor (1 shared paper)M. Flint Beal (9 shared papers)Merit Cudkowicz (31 shared papers)
- Journals
- Neurology (28 papers)Annals of Neurology (25 papers)Proceedings of the National Academy of Sciences (16 papers)Human Molecular Genetics (13 papers)Nature Genetics (12 papers)
- Partner nations
- United StatesUnited KingdomItaly
In The Last Decade
Robert H. Brown
399 papers receiving 48.4k citations
Robert H. Brown's Hit Papers
Peers
Comparison fields: 5 of 192
- Neurology 24.5k
- Genetics 12.8k
- Neurology 6.6k
- Cellular and Molecular Neuroscience 8.2k
- Molecular Biology 23.7k
Countries citing papers authored by Robert H. Brown
This map shows the geographic impact of Robert H. Brown's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Robert H. Brown with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Robert H. Brown more than expected).
Fields of papers citing papers by Robert H. Brown
This network shows the impact of papers produced by Robert H. Brown. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Robert H. Brown. The network helps show where Robert H. Brown may publish in the future.
Co-authors
The 25 scholars most cited alongside Robert H. Brown, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
Showing the 20 most-cited of 408 papers — load more, or switch the sort, to bring in the rest.
| # | Work | ||
|---|---|---|---|
| 1 | Dystrophin: The protein product of the duchenne muscular dystrophy locus Hit paper breakdown → | 1987 | 4003 |
| 2 | Mutations in the FUS/TLS Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis Hit paper breakdown → | 2009 | 2168 |
| 3 | Decoding ALS: from genes to mechanism Hit paper breakdown → | 2016 | 1615 |
| 4 | Amyotrophic Lateral Sclerosis Hit paper breakdown → | 2017 | 1430 |
| 5 | Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury Hit paper breakdown → | 1996 | 1047 |
| 6 | Molecular biology of amyotrophic lateral sclerosis: insights from genetics Hit paper breakdown → | 2006 | 963 |
| 7 | Wild-Type Nonneuronal Cells Extend Survival of SOD1 Mutant Motor Neurons in ALS Mice Hit paper breakdown → | 2003 | 928 |
| 8 | Mutant dynactin in motor neuron disease Hit paper breakdown → | 2003 | 824 |
| 9 | Characterization of Dystrophin in Muscle-Biopsy Specimens from Patients with Duchenne's or Becker's Muscular Dystrophy Hit paper breakdown → | 1988 | 807 |
| 10 | Exome sequencing in amyotrophic lateral sclerosis identifies risk genes and pathways Hit paper breakdown → | 2015 | 801 |
| 11 | Dysferlin, a novel skeletal muscle gene, is mutated in Miyoshi myopathy and limb girdle muscular dystrophy Hit paper breakdown → | 1998 | 754 |
| 12 | Efficacy and safety of minimally invasive surgery with thrombolysis in intracerebral haemorrhage evacuation (MISTIE III): a randomised, controlled, open-label, blinded endpoint phase 3 trial Hit paper breakdown → | 2019 | 642 |
| 13 | Wild-type and mutant SOD1 share an aberrant conformation and a common pathogenic pathway in ALS Hit paper breakdown → | 2010 | 585 |
| 14 | 2006 | 579 | |
| 15 | 1993 | 551 | |
| 16 | 2012 | 548 | |
| 17 | Intrinsic Membrane Hyperexcitability of Amyotrophic Lateral Sclerosis Patient-Derived Motor Neurons Hit paper breakdown → | 2014 | 534 |
| 18 | Genome-wide Analyses Identify KIF5A as a Novel ALS Gene Hit paper breakdown → | 2018 | 526 |
| 19 | 1997 | 521 | |
| 20 | Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis Hit paper breakdown → | 2016 | 453 |
About Robert H. Brown
Robert H. Brown is a scholar working on Neurology, Genetics, Neurology, Cellular and Molecular Neuroscience and Molecular Biology, having authored 408 papers that have together received 50.1k indexed citations. Recurring topics across this work include Amyotrophic Lateral Sclerosis Research (230 papers), Neurogenetic and Muscular Disorders Research (141 papers), Parkinson's Disease Mechanisms and Treatments (46 papers), Neurological diseases and metabolism (46 papers), Muscle Physiology and Disorders (37 papers), Genetic Neurodegenerative Diseases (26 papers), Prion Diseases and Protein Misfolding (21 papers) and Ion channel regulation and function (19 papers). The work is most often cited by research in Neurology (24.5k citations), Genetics (12.8k citations), Neurology (6.6k citations), Cellular and Molecular Neuroscience (8.2k citations) and Molecular Biology (23.7k citations). Robert H. Brown has collaborated with scholars based in United States, United Kingdom and Italy. Frequent co-authors include Eric Hoffman, Louis M. Kunkel, Piera Pasinelli, Ammar Al‐Chalabi, Don W. Cleveland, J. Paul Taylor, M. Flint Beal, Merit Cudkowicz, Robert J. Ferrante and Diane M. McKenna-Yasek. Their work appears in journals such as Neurology, Annals of Neurology, Proceedings of the National Academy of Sciences, Human Molecular Genetics and Nature Genetics.
Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.