H. Bernheimer
- Clinical Biochemistry top 2%
- Metabolism and Genetic Disorders 10
- Neurology top 5%
- Peripheral Neuropathies and Disorders 11
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- Hereditary Neurological Disorders 9
- Physiology top 10%
- Lysosomal Storage Disorders Research 9
- Adipose Tissue and Metabolism 9
- Biochemistry top 5%
- Eicosanoids and Hypertension Pharmacology 5
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- Peroxisome Proliferator-Activated Receptors 17
- Glycosylation and Glycoproteins Research 11
H. Bernheimer
64 papers receiving 1.3k citations
Peers
Comparison fields: 5 of 94
- Clinical Biochemistry 158
- Neurology 346
- Cellular and Molecular Neuroscience 297
- Physiology 363
- Biochemistry 85
Countries citing papers authored by H. Bernheimer
This map shows the geographic impact of H. Bernheimer'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 H. Bernheimer with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites H. Bernheimer more than expected).
Fields of papers citing papers by H. Bernheimer
This network shows the impact of papers produced by H. Bernheimer. 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 H. Bernheimer. The network helps show where H. Bernheimer may publish in the future.
Co-authorship network
The 25 scholars most cited alongside H. Bernheimer, 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 | 2010 | 7 | |
| 2 | 2008 | 28 | |
| 3 | 2007 | 7 | |
| 4 | 2005 | 23 | |
| 5 | 2000 | 16 | |
| 6 | 2000 | 24 | |
| 7 | 1998 | 6 | |
| 8 | 1997 | 2 | |
| 9 | 1997 | 170 | |
| 10 | 1996 | 27 | |
| 11 | 1995 | 1 | |
| 12 | 1995 | 14 | |
| 13 | 1993 | 1 | |
| 14 | 1993 | 13 | |
| 15 | 1989 | 6 | |
| 16 | 1988 | 6 | |
| 17 | 1987 | 17 | |
| 18 | 1985 | 18 | |
| 19 | Antibodies in the pathogenesis of demyelination in chronic relapsing EAE (cr-EAE). | 1984 | 12 |
| 20 | [On the behavior of brain gangliosides in 2 cases of late infantile amaurotic idiocy]. | 1968 | 18 |
About H. Bernheimer
H. Bernheimer is a scholar working on Clinical Biochemistry, Neurology and Physiology, having authored 65 papers that have together received 1.4k indexed citations. Recurring topics across this work include Peroxisome Proliferator-Activated Receptors (17 papers), Glycosylation and Glycoproteins Research (11 papers), Peripheral Neuropathies and Disorders (11 papers), Metabolism and Genetic Disorders (10 papers), Hereditary Neurological Disorders (9 papers), Lysosomal Storage Disorders Research (9 papers), Adipose Tissue and Metabolism (9 papers) and Eicosanoids and Hypertension Pharmacology (5 papers). The work is most often cited by research in Clinical Biochemistry (158 citations), Neurology (346 citations) and Cellular and Molecular Neuroscience (297 citations). H. Bernheimer has collaborated with scholars based in Austria, United States and Germany. Frequent co-authors include B. Schwerer, Oleh Hornykiewicz, W Birkmayer, Brunhilde Molzer, Hans Lassmann, Johannes Berger, Herbert Budka, K. Kitz, Anthony P. Moran and Markus H. Schwab. Their work appears in journals such as Clinica Chimica Acta, Acta Neuropathologica, Journal of Molecular Medicine, Infection and Immunity and Annals of the New York Academy of Sciences.
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.