Barbara E. Stopschinski

479 citations
8 papers · 371 · h-index 7

Impact in

  • Neurology top 10%
    • Parkinson's Disease Mechanisms and Treatments
    • Neuroinflammation and Neurodegeneration Mechanisms
    • Neurological diseases and metabolism
    • Alzheimer's disease research and treatments

Papers in

    • Prion Diseases and Protein Misfolding 2
    • Wnt/β-catenin signaling in development and cancer 1
    • Cellular Mechanics and Interactions 2

Barbara E. Stopschinski

8 papers receiving 365 citations

Peers

Barbara E. Stopschinski
Comparison fields: 5 of 69
  • Neurology 78
  • Physiology 145
  • Cell Biology 84
  • Neurology 72
  • Genetics 40
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Citations per year

Countries citing papers authored by Barbara E. Stopschinski

Since Specialization
Citations

This map shows the geographic impact of Barbara E. Stopschinski'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 Barbara E. Stopschinski with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Barbara E. Stopschinski more than expected).

Fields of papers citing papers by Barbara E. Stopschinski

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Barbara E. Stopschinski. 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 Barbara E. Stopschinski. The network helps show where Barbara E. Stopschinski may publish in the future.

Co-authors

The 25 scholars most cited alongside Barbara E. Stopschinski, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.

Border = papers with Barbara E. Stopschinski Line = papers co-authored together Barbara E. Stopschinski links everyone, so they are left out of the graph.

All Works

8 of 8 papers shown
#Work
1 2018133
2 201799
3 201260
4 202024
5 202120
6 201118
7 201415
8 20122

About Barbara E. Stopschinski

Barbara E. Stopschinski is a scholar working on Molecular Biology, Cell Biology, Physiology, Genetics and Cancer Research, having authored 8 papers that have together received 371 indexed citations. Recurring topics across this work include Alzheimer's disease research and treatments (3 papers), Prion Diseases and Protein Misfolding (2 papers), Cellular Mechanics and Interactions (2 papers), Neurological diseases and metabolism (1 paper), Cancer Genomics and Diagnostics (1 paper), Cardiovascular Effects of Exercise (1 paper), Wnt/β-catenin signaling in development and cancer (1 paper) and Advanced Fluorescence Microscopy Techniques (1 paper). The work is most often cited by research in Neurology (78 citations), Physiology (145 citations), Cell Biology (84 citations), Neurology (72 citations) and Genetics (40 citations). Barbara E. Stopschinski has collaborated with scholars based in Germany, United States and Switzerland. Frequent co-authors include Marc I. Diamond, Dagmar Beier, Christoph P. Beier, Brandon B. Holmes, Gregory M. Miller, Linda C. Hsieh‐Wilson, Jaime Vaquer‐Alicea, Sandi Jo Estill, André Schönichen and Matthias Geyer. Their work appears in journals such as Journal of Biological Chemistry, The Lancet Neurology, Acta Neuropathologica Communications, Cancer Letters and European Journal of Cell Biology.

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.

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