Michael W. Sereda

7.0k total citations · 2 hit papers
48 papers, 4.6k citations indexed

About

Michael W. Sereda is a scholar working on Cellular and Molecular Neuroscience, Neurology and Neurology. According to data from OpenAlex, Michael W. Sereda has authored 48 papers receiving a total of 4.6k indexed citations (citations by other indexed papers that have themselves been cited), including 41 papers in Cellular and Molecular Neuroscience, 15 papers in Neurology and 13 papers in Neurology. Recurrent topics in Michael W. Sereda's work include Hereditary Neurological Disorders (35 papers), Nerve injury and regeneration (16 papers) and Neurological diseases and metabolism (10 papers). Michael W. Sereda is often cited by papers focused on Hereditary Neurological Disorders (35 papers), Nerve injury and regeneration (16 papers) and Neurological diseases and metabolism (10 papers). Michael W. Sereda collaborates with scholars based in Germany, United Kingdom and Switzerland. Michael W. Sereda's co-authors include Klaus‐Armin Nave, Bastian G. Brinkmann, Ueli Suter, Markus H. Schwab, Dies Meijer, Cary Lai, Tobias M. Fischer, Carmen Birchmeier, Ruth M. Stassart and Sandra Goebbels and has published in prestigious journals such as Nature, Science and Proceedings of the National Academy of Sciences.

In The Last Decade

Michael W. Sereda

48 papers receiving 4.5k citations

Hit Papers

Glycolytic oligodendrocytes maintain myelin and long-te... 2004 2026 2011 2018 2012 2004 250 500 750 1000

Peers

Michael W. Sereda
Michael W. Sereda
Citations per year, relative to Michael W. Sereda Michael W. Sereda (= 1×) peers Markus H. Schwab

Countries citing papers authored by Michael W. Sereda

Since Specialization
Citations

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

Fields of papers citing papers by Michael W. Sereda

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Michael W. Sereda. 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 Michael W. Sereda. The network helps show where Michael W. Sereda may publish in the future.

Co-authorship network of co-authors of Michael W. Sereda

This figure shows the co-authorship network connecting the top 25 collaborators of Michael W. Sereda. A scholar is included among the top collaborators of Michael W. Sereda 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 Michael W. Sereda. Michael W. Sereda is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Kungl, Theresa, Gesine Saher, Robert Fledrich, et al.. (2024). Targeting PI3K/Akt/mTOR signaling in rodent models of PMP22 gene-dosage diseases. EMBO Molecular Medicine. 16(3). 616–640. 5 indexed citations
2.
Siems, Sophie B., Olaf Jahn, Nirmal Kannaiyan, et al.. (2020). Proteome profile of peripheral myelin in healthy mice and in a neuropathy model. eLife. 9. 55 indexed citations
3.
Vingill, Siv, Olaf Jahn, Robert Fledrich, et al.. (2019). Myelinating Glia-Specific Deletion of Fbxo7 in Mice Triggers Axonal Degeneration in the Central Nervous System Together with Peripheral Neuropathy. Journal of Neuroscience. 39(28). 5606–5626. 10 indexed citations
4.
Sociali, Giovanna, Thomas Prukop, Ilaria Cervellini, et al.. (2016). Tolerability and efficacy study of P2X7 inhibition in experimental Charcot-Marie-Tooth type 1A (CMT1A) neuropathy. Neurobiology of Disease. 95. 145–157. 25 indexed citations
5.
Quintes, Susanne, Bastian G. Brinkmann, Franziska Fröb, et al.. (2016). Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair. Nature Neuroscience. 19(8). 1050–1059. 114 indexed citations
6.
Ekins, Sean, Nadia K. Litterman, Renée J.G. Arnold, et al.. (2015). A brief review of recent Charcot-Marie-Tooth research and priorities. F1000Research. 4. 53–53. 30 indexed citations
7.
Pehli̇van, Davut, Christine R. Beck, Yuji Okamoto, et al.. (2015). The role of combined SNV and CNV burden in patients with distal symmetric polyneuropathy. Genetics in Medicine. 18(5). 443–451. 14 indexed citations
8.
Fledrich, Robert, Ruth M. Stassart, Thomas Prukop, et al.. (2014). Soluble neuregulin-1 modulates disease pathogenesis in rodent models of Charcot-Marie-Tooth disease 1A. Nature Medicine. 20(9). 1055–1061. 134 indexed citations
9.
Prukop, Thomas, Sven P. Wichert, Robert Fledrich, et al.. (2014). Progesterone Antagonist Therapy in a Pelizaeus-Merzbacher Mouse Model. The American Journal of Human Genetics. 94(4). 533–546. 22 indexed citations
10.
Makoukji, Joelle, Martin Belle, Delphine Meffre, et al.. (2012). Lithium enhances remyelination of peripheral nerves. Proceedings of the National Academy of Sciences. 109(10). 3973–3978. 83 indexed citations
11.
Stassart, Ruth M., Robert Fledrich, Viktorija Velanac, et al.. (2012). A role for Schwann cell–derived neuregulin-1 in remyelination. Nature Neuroscience. 16(1). 48–54. 219 indexed citations
12.
Fledrich, Robert, Ruth M. Stassart, & Michael W. Sereda. (2012). Murine therapeutic models for Charcot-Marie-Tooth (CMT) disease. British Medical Bulletin. 102(1). 89–113. 46 indexed citations
13.
Fledrich, Robert, Beate Schlotter‐Weigel, Sven P. Wichert, et al.. (2011). A rat model of Charcot–Marie–Tooth disease 1A recapitulates disease variability and supplies biomarkers of axonal loss in patients. Brain. 135(1). 72–87. 36 indexed citations
14.
Wessig, Carsten, Leonie Jestaedt, Michael W. Sereda, Martin Bendszus, & Guido Stoll. (2007). Gadofluorine M-enhanced magnetic resonance nerve imaging: Comparison between acute inflammatory and chronic degenerative demyelination in rats. Experimental Neurology. 210(1). 137–143. 28 indexed citations
15.
Nave, Klaus‐Armin, Michael W. Sereda, & Hannelore Ehrenreich. (2007). Mechanisms of Disease: inherited demyelinating neuropathies—from basic to clinical research. Nature Clinical Practice Neurology. 3(8). 453–464. 81 indexed citations
16.
Hörste, Gerd Meyer zu, Thomas Prukop, Klaus‐Armin Nave, & Michael W. Sereda. (2006). Myelin Disorders: Causes and Perspectives of Charcot-Marie-Tooth Neuropathy. Journal of Molecular Neuroscience. 28(1). 77–88. 15 indexed citations
17.
Michailov, G., Michael W. Sereda, Bastian G. Brinkmann, et al.. (2004). Axonal Neuregulin-1 Regulates Myelin Sheath Thickness. Science. 304(5671). 700–703. 730 indexed citations breakdown →
18.
Grandis, Marina, Massimo Leandri, Tiziana Vigo, et al.. (2004). Early abnormalities in sciatic nerve function and structure in a rat model of Charcot-Marie-Tooth type 1A disease. Experimental Neurology. 190(1). 213–223. 17 indexed citations
19.
Sereda, Michael W., et al.. (2003). Therapeutic administration of progesterone antagonist in a model of Charcot-Marie-Tooth disease (CMT-1A). Nature Medicine. 9(12). 1533–1537. 217 indexed citations
20.
Sereda, Michael W., Ian R. Griffiths, Helen Stewart, et al.. (1996). A Transgenic Rat Model of Charcot-Marie-Tooth Disease. Neuron. 16(5). 1049–1060. 281 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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