Matthias Elstner

2.1k total citations
31 papers, 1.2k citations indexed

About

Matthias Elstner is a scholar working on Molecular Biology, Cellular and Molecular Neuroscience and Neurology. According to data from OpenAlex, Matthias Elstner has authored 31 papers receiving a total of 1.2k indexed citations (citations by other indexed papers that have themselves been cited), including 19 papers in Molecular Biology, 8 papers in Cellular and Molecular Neuroscience and 7 papers in Neurology. Recurrent topics in Matthias Elstner's work include Mitochondrial Function and Pathology (14 papers), Metabolism and Genetic Disorders (7 papers) and Parkinson's Disease Mechanisms and Treatments (6 papers). Matthias Elstner is often cited by papers focused on Mitochondrial Function and Pathology (14 papers), Metabolism and Genetic Disorders (7 papers) and Parkinson's Disease Mechanisms and Treatments (6 papers). Matthias Elstner collaborates with scholars based in Germany, United Kingdom and United States. Matthias Elstner's co-authors include Andreas Bender, Thomas Klopstock, Christopher M. Morris, Holger Prokisch, Douglass M. Turnbull, Thomas Meitinger, Arthur E. Oakley, Joanna F. Collingwood, J.A. Edwardson and Jon Dobson and has published in prestigious journals such as Brain, Neurology and Annals of Neurology.

In The Last Decade

Matthias Elstner

31 papers receiving 1.2k citations

Peers

Matthias Elstner
Francesca De Giorgi France
Yang Yuan United States
C. Thong United States
Mügen Terzioglu Finland
Diane T. W. Chang United States
Victor S. Van Laar United States
Pilar González‐Cabo Spain
Julia C. Fitzgerald Germany
Tatiana R. Rosenstock Brazil
Simone Bido Italy
Francesca De Giorgi France
Matthias Elstner
Citations per year, relative to Matthias Elstner Matthias Elstner (= 1×) peers Francesca De Giorgi

Countries citing papers authored by Matthias Elstner

Since Specialization
Citations

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

Fields of papers citing papers by Matthias Elstner

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Matthias Elstner

This figure shows the co-authorship network connecting the top 25 collaborators of Matthias Elstner. A scholar is included among the top collaborators of Matthias Elstner 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 Matthias Elstner. Matthias Elstner 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
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Ban, Rui, Zhimei Liu, Masaru Shimura, et al.. (2021). Biallelic COA7-Variants Leading to Developmental Regression With Progressive Spasticity and Brain Atrophy in a Chinese Patient. Frontiers in Genetics. 12. 685035–685035. 6 indexed citations
3.
Hotter, Benjamin, Benno Ikenberg, Martin Ritter, et al.. (2021). Positionspapier Schlaganfallnachsorge der Deutschen Schlaganfall-Gesellschaft – Teil 2: Konzept für eine umfassende Schlaganfallnachsorge. Der Nervenarzt. 93(4). 377–384. 2 indexed citations
4.
Kopajtich, Robert, Matthias Elstner, Hua Li, et al.. (2021). Identification of a novel m.3955G > A variant in MT-ND1 associated with Leigh syndrome. Mitochondrion. 62. 13–23. 4 indexed citations
5.
Kopajtich, Robert, Matthias Elstner, Zhaoxia Wang, et al.. (2021). Identification of a Novel Variant in MT-CO3 Causing MELAS. Frontiers in Genetics. 12. 638749–638749. 5 indexed citations
6.
Schwarzbach, Christopher, Dominik Michalski, Markus Wagner, et al.. (2021). Positionspapier Schlaganfallnachsorge der Deutschen Schlaganfall-Gesellschaft – Teil 3: Strukturelle Konzepte für zukünftige Versorgungsformen der Schlaganfallnachsorge. Der Nervenarzt. 93(4). 385–391. 1 indexed citations
7.
Brosel, Sonja, et al.. (2015). Molecular aging of the mammalian vestibular system. Ageing Research Reviews. 26. 72–80. 29 indexed citations
8.
Perier, Céline, Andreas Bender, Elena García‐Arumí, et al.. (2013). Accumulation of mitochondrial DNA deletions within dopaminergic neurons triggers neuroprotective mechanisms. Brain. 136(8). 2369–2378. 58 indexed citations
9.
Elstner, Matthias, Sarina Müller, Falk Schlaudraff, et al.. (2011). Neuromelanin, neurotransmitter status and brainstem location determine the differential vulnerability of catecholaminergic neurons to mitochondrial DNA deletions. Molecular Brain. 4(1). 43–43. 38 indexed citations
10.
Elstner, Matthias & Douglass M. Turnbull. (2011). Transcriptome analysis in mitochondrial disorders. Brain Research Bulletin. 88(4). 285–293. 13 indexed citations
11.
Elstner, Matthias, Christopher M. Morris, Katharina Heim, et al.. (2011). Expression analysis of dopaminergic neurons in Parkinson’s disease and aging links transcriptional dysregulation of energy metabolism to cell death. Acta Neuropathologica. 122(1). 75–86. 123 indexed citations
12.
Elstner, Matthias, Christophe Andréoli, Thomas Klopstock, Thomas Meitinger, & Holger Prokisch. (2009). Chapter 1 The Mitochondrial Proteome Database. Methods in enzymology on CD-ROM/Methods in enzymology. 457. 3–20. 64 indexed citations
13.
Swalwell, Helen, Emma L. Blakely, Katarzyna Tońska, et al.. (2008). A homoplasmic mtDNA variant can influence the phenotype of the pathogenic m.7472Cins MTTS1 mutation: are two mutations better than one?. European Journal of Human Genetics. 16(10). 1265–1274. 28 indexed citations
14.
Bender, Andreas, W. Samtleben, Matthias Elstner, & Thomas Klopstock. (2008). Long-term creatine supplementation is safe in aged patients with Parkinson disease. Nutrition Research. 28(3). 172–178. 53 indexed citations
15.
Elstner, Matthias, Caroline Schmidt, Holger Prokisch, et al.. (2008). Mitochondrial 12S rRNA susceptibility mutations in aminoglycoside-associated and idiopathic bilateral vestibulopathy. Biochemical and Biophysical Research Communications. 377(2). 379–383. 19 indexed citations
16.
Elstner, Matthias, Christophe Andréoli, Uwe Ahting, et al.. (2008). MitoP2: An Integrative Tool for the Analysis of the Mitochondrial Proteome. Molecular Biotechnology. 40(3). 306–315. 49 indexed citations
17.
Rupprecht, Tobias A., et al.. (2008). Autoimmune‐mediated polyneuropathy triggered by borrelial infection?. Muscle & Nerve. 37(6). 781–785. 17 indexed citations
18.
Oakley, Arthur E., Joanna F. Collingwood, Jon Dobson, et al.. (2007). Individual dopaminergic neurons show raised iron levels in Parkinson disease. Neurology. 68(21). 1820–1825. 225 indexed citations
19.
Bender, Andreas, Matthias Elstner, Robert Paul, & Andreas Straube. (2004). Severe symptomatic aseptic chemical meningitis following myelography. Neurology. 63(7). 1311–1313. 11 indexed citations
20.
Tatton, W. G., Ruth M.E. Chalmers-Redman, Matthias Elstner, et al.. (2000). Glyceraldehyde-3-phosphate dehydrogenase in neurodegeneration and apoptosis signaling. PubMed. 77–100. 81 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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