Roberth Byström
Impact in
- Neurology top 5%
- Amyotrophic Lateral Sclerosis Research
- Parkinson's Disease Mechanisms and Treatments
- Neurological diseases and metabolism
- Physiology top 10%
- Alzheimer's disease research and treatments
Papers in
-
- Prion Diseases and Protein Misfolding 2
- Microbial Metabolic Engineering and Bioproduction 1
- Mitochondrial Function and Pathology 1
- Lipid Membrane Structure and Behavior 1
-
- Alzheimer's disease research and treatments 4
- Co-authors
- Mikael Oliveberg (2 shared papers)Peter M. Andersen (2 shared papers)Gerhard Gröbner (3 shared papers)Niklas Boknäs (1 shared paper)Mikael Lindberg (1 shared paper)Marcus Bokvist (2 shared papers)Christopher Aisenbrey (2 shared papers)Tomasz Borowik (2 shared papers)
In The Last Decade
Roberth Byström
6 papers receiving 517 citations
Peers
Comparison fields: 5 of 65
- Neurology 248
- Physiology 201
- Neurology 61
- Biomaterials 82
- Genetics 59
Countries citing papers authored by Roberth Byström
This map shows the geographic impact of Roberth Byström'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 Roberth Byström with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Roberth Byström more than expected).
Fields of papers citing papers by Roberth Byström
This network shows the impact of papers produced by Roberth Byström. 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 Roberth Byström. The network helps show where Roberth Byström may publish in the future.
Co-authors
The 21 scholars most cited alongside Roberth Byström, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2005 | 196 | |
| 2 | 2007 | 167 | |
| 3 | 2010 | 84 | |
| 4 | 2008 | 41 | |
| 5 | 2016 | 33 | |
| 6 | SOD1´s Law : An Investigation of ALS Provoking Properties in SOD1 | 2009 | 1 |
About Roberth Byström
Roberth Byström is a scholar working on Molecular Biology, Physiology, Neurology, Cellular and Molecular Neuroscience and Cell Biology, having authored 6 papers that have together received 522 indexed citations. Recurring topics across this work include Alzheimer's disease research and treatments (4 papers), Amyotrophic Lateral Sclerosis Research (3 papers), Prion Diseases and Protein Misfolding (2 papers), Parkinson's Disease Mechanisms and Treatments (1 paper), Microbial Metabolic Engineering and Bioproduction (1 paper), Mitochondrial Function and Pathology (1 paper), Genetic Neurodegenerative Diseases (1 paper) and Lipid Membrane Structure and Behavior (1 paper). The work is most often cited by research in Neurology (248 citations), Physiology (201 citations), Neurology (61 citations), Biomaterials (82 citations) and Genetics (59 citations). Roberth Byström has collaborated with scholars based in Sweden, Poland and Norway. Frequent co-authors include Mikael Oliveberg, Peter M. Andersen, Gerhard Gröbner, Niklas Boknäs, Mikael Lindberg, Marcus Bokvist, Christopher Aisenbrey, Tomasz Borowik, Fredrick Lindström and Marc‐Antoine Sani. Their work appears in journals such as European Biophysics Journal, Proceedings of the National Academy of Sciences, Cell Biochemistry and Biophysics, Biofuels Bioproducts and Biorefining and Journal of Biological Chemistry.
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.