Birgit Schwalenstöcker

1.1k total citations
16 papers, 745 citations indexed

About

Birgit Schwalenstöcker is a scholar working on Molecular Biology, Neurology and Genetics. According to data from OpenAlex, Birgit Schwalenstöcker has authored 16 papers receiving a total of 745 indexed citations (citations by other indexed papers that have themselves been cited), including 13 papers in Molecular Biology, 11 papers in Neurology and 6 papers in Genetics. Recurrent topics in Birgit Schwalenstöcker's work include Amyotrophic Lateral Sclerosis Research (11 papers), Neurogenetic and Muscular Disorders Research (5 papers) and Prion Diseases and Protein Misfolding (4 papers). Birgit Schwalenstöcker is often cited by papers focused on Amyotrophic Lateral Sclerosis Research (11 papers), Neurogenetic and Muscular Disorders Research (5 papers) and Prion Diseases and Protein Misfolding (4 papers). Birgit Schwalenstöcker collaborates with scholars based in Germany, France and Poland. Birgit Schwalenstöcker's co-authors include Albert C. Ludolph, Thomas Meyer, Christoph Münch, Stefan Stamm, Jean‐Philippe Loeffler, Caterina Bendotti, Susanne Petri, Pierre‐François Pradat, Linda Greensmith and Markus A. Rüegg and has published in prestigious journals such as Journal of Neurochemistry, Human Molecular Genetics and American Journal Of Pathology.

In The Last Decade

Birgit Schwalenstöcker

16 papers receiving 727 citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Birgit Schwalenstöcker Germany 13 436 327 289 248 95 16 745
Anissa Fergani France 10 635 1.5× 271 0.8× 373 1.3× 157 0.6× 85 0.9× 10 843
Javier H. Jara United States 14 434 1.0× 249 0.8× 271 0.9× 175 0.7× 140 1.5× 15 677
Raquel Castellanos United States 9 300 0.7× 286 0.9× 158 0.5× 198 0.8× 178 1.9× 15 691
Hélène Tran France 10 616 1.4× 523 1.6× 332 1.1× 241 1.0× 70 0.7× 16 933
Bhuvaneish T. Selvaraj United Kingdom 15 317 0.7× 354 1.1× 174 0.6× 164 0.7× 130 1.4× 30 709
Tijs Vandoorne Belgium 9 377 0.9× 325 1.0× 220 0.8× 111 0.4× 63 0.7× 12 648
Gabrielle Gardian United States 7 440 1.0× 302 0.9× 96 0.3× 266 1.1× 131 1.4× 8 704
Amanda M. Gleixner United States 15 300 0.7× 492 1.5× 159 0.6× 96 0.4× 46 0.5× 20 714
Virginia Le Verche United States 8 248 0.6× 274 0.8× 154 0.5× 111 0.4× 124 1.3× 9 562
Kerstin E. Braunstein United States 13 267 0.6× 275 0.8× 159 0.6× 97 0.4× 100 1.1× 13 581

Countries citing papers authored by Birgit Schwalenstöcker

Since Specialization
Citations

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

Fields of papers citing papers by Birgit Schwalenstöcker

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Birgit Schwalenstöcker. 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 Birgit Schwalenstöcker. The network helps show where Birgit Schwalenstöcker may publish in the future.

Co-authorship network of co-authors of Birgit Schwalenstöcker

This figure shows the co-authorship network connecting the top 25 collaborators of Birgit Schwalenstöcker. A scholar is included among the top collaborators of Birgit Schwalenstöcker based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Birgit Schwalenstöcker. Birgit Schwalenstöcker is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

16 of 16 papers shown
1.
Eschbach, J. W., Birgit Schwalenstöcker, Selma M. Soyal, et al.. (2013). PGC-1  is a male-specific disease modifier of human and experimental amyotrophic lateral sclerosis. Human Molecular Genetics. 22(17). 3477–3484. 69 indexed citations
2.
Eschbach, Judith, Diana Wiesner, Birgit Schwalenstöcker, et al.. (2013). Full-length PGC-1α salvages the phenotype of a mouse model of human neuropathy through mitochondrial proliferation. Human Molecular Genetics. 22(25). 5096–5106. 3 indexed citations
3.
Fergani, Anissa, Judith Eschbach, Hugues Oudart, et al.. (2011). A mutation in the dynein heavy chain gene compensates for energy deficit of mutant SOD1 mice and increases potentially neuroprotective IGF-1. Molecular Neurodegeneration. 6(1). 26–26. 13 indexed citations
4.
Ludolph, Albert C., Caterina Bendotti, Eran Blaugrund, et al.. (2010). Guidelines for preclinical animal research in ALS/MND: A consensus meeting. Amyotrophic Lateral Sclerosis. 11(1-2). 38–45. 239 indexed citations
5.
Eschbach, Judith, Anissa Fergani, Hugues Oudart, et al.. (2010). Mutations in cytoplasmic dynein lead to a Huntington's disease-like defect in energy metabolism of brown and white adipose tissues. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1812(1). 59–69. 18 indexed citations
6.
Steinacker, Petra, Stefan Lehnert, Olaf Jahn, et al.. (2010). Neuroprotective Function of Cellular Prion Protein in a Mouse Model of Amyotrophic Lateral Sclerosis. American Journal Of Pathology. 176(3). 1409–1420. 24 indexed citations
7.
Dupuis, Luc, Anissa Fergani, Kerstin E. Braunstein, et al.. (2008). Mice with a mutation in the dynein heavy chain 1 gene display sensory neuropathy but lack motor neuron disease. Experimental Neurology. 215(1). 146–152. 45 indexed citations
8.
Barańczyk‐Kuźma, Anna, et al.. (2007). Age-related Changes in Tau Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis. Neurochemical Research. 32(3). 415–421. 10 indexed citations
9.
Habisch, Hansjörg, Mirosław Janowski, Aleksandra Habich, et al.. (2007). Intrathecal application of neuroectodermally converted stem cells into a mouse model of ALS: limited intraparenchymal migration and survival narrows therapeutic effects. Journal of Neural Transmission. 114(11). 1395–1406. 95 indexed citations
10.
Habisch, Hansjörg, Birgit Schwalenstöcker, Ruth Danzeisen, et al.. (2007). Limited effects of glatiramer acetate in the high-copy number hSOD1-G93A mouse model of ALS. Experimental Neurology. 206(2). 288–295. 20 indexed citations
11.
Kuźma‐Kozakiewicz, Magdalena, Birgit Schwalenstöcker, Beata Kaźmierczak, et al.. (2006). Tau Isoforms Expression in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis. Neurochemical Research. 31(5). 597–602. 5 indexed citations
12.
Münch, Christoph, Stefan Stamm, Birgit Schwalenstöcker, et al.. (2003). Differential regulation of 5′ splice variants of the glutamate transporter EAAT2 in an in vivo model of chemical hypoxia induced by 3‐nitropropionic acid. Journal of Neuroscience Research. 71(6). 819–825. 24 indexed citations
13.
Münch, Christoph, Benzhong Zhu, Stefan Stamm, et al.. (2002). Alternative splicing of the 5′‐sequences of the mouse EAAT2 glutamate transporter and expression in a transgenic model for amyotrophic lateral sclerosis. Journal of Neurochemistry. 82(3). 594–603. 36 indexed citations
14.
Münch, Christoph, et al.. (2000). Differential RNA cleavage and polyadenylation of the glutamate transporter EAAT2 in the human brain. Molecular Brain Research. 80(2). 244–251. 18 indexed citations
15.
Meyer, Thomas, Christoph Münch, Birgit Schwalenstöcker, et al.. (1999). The RNA of the glutamate transporter EAAT2 is variably spliced in amyotrophic lateral sclerosis and normal individuals. Journal of the Neurological Sciences. 170(1). 45–50. 105 indexed citations
16.
Münch, Christoph, et al.. (1998). 5′-Heterogeneity of the human excitatory amino acid transporter cDNA EAAT2 (GLT-1). Neuroreport. 9(7). 1295–1297. 21 indexed citations

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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