Inge E. Krabbendam

492 citations
11 papers · 352 indexed · h-index 10

Impact in

Papers in

    • Ion channel regulation and function 4
    • Mitochondrial Function and Pathology 4
    • Genomics, phytochemicals, and oxidative stress 2
    • Neuroscience and Neuropharmacology Research 4
    • Genetic Neurodegenerative Diseases 2

Inge E. Krabbendam

11 papers receiving 350 citations

Peers

Inge E. Krabbendam
Comparison fields: 5 of 70
  • Cellular and Molecular Neuroscience 127
  • Molecular Biology 255
  • Aging 6
  • Developmental Neuroscience 13
  • Neurology 24
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Citations per field
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Citations per year

Countries citing papers authored by Inge E. Krabbendam

Since Specialization
Citations

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

Fields of papers citing papers by Inge E. Krabbendam

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authors

The 25 scholars most cited alongside Inge E. Krabbendam, 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 Inge E. Krabbendam Line = papers co-authored together Inge E. Krabbendam links everyone, so they are left out of the graph.

All Works

11 of 11 papers shown
#Work
1 201777
2 201754
3 202038
4 201737
5 202031
6 202330
7 202028
8 201822
9 201920
10 201811
11 20214

About Inge E. Krabbendam

Inge E. Krabbendam is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience, Pathology and Forensic Medicine, Neurology and Cardiology and Cardiovascular Medicine, having authored 11 papers that have together received 352 indexed citations. Recurring topics across this work include Ion channel regulation and function (4 papers), Mitochondrial Function and Pathology (4 papers), Neuroscience and Neuropharmacology Research (4 papers), Genomics, phytochemicals, and oxidative stress (2 papers), Genetic Neurodegenerative Diseases (2 papers), Cardiac electrophysiology and arrhythmias (1 paper), MicroRNA in disease regulation (1 paper) and Alzheimer's disease research and treatments (1 paper). The work is most often cited by research in Cellular and Molecular Neuroscience (127 citations), Molecular Biology (255 citations), Aging (6 citations), Developmental Neuroscience (13 citations) and Neurology (24 citations). Inge E. Krabbendam has collaborated with scholars based in Netherlands, Germany and United States. Frequent co-authors include Amalia M. Dolga, Carsten Culmsee, Birgit Honrath, Marina Trombetta-Lima, Michelle A. Poirier, Zhipeng Hou, Jennifer C. Boatz, Ronald Wetzel, Ravindra Kodali and Patrick C.A. van der Wel. Their work appears in journals such as Cell Death and Disease, Nature Communications, Cell Calcium, The International Journal of Biochemistry & Cell Biology and Neurology 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.

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