Benjamin Schmid

3.5k total citations · 1 hit paper
60 papers, 1.9k citations indexed

About

Benjamin Schmid is a scholar working on Molecular Biology, Physiology and Cellular and Molecular Neuroscience. According to data from OpenAlex, Benjamin Schmid has authored 60 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 37 papers in Molecular Biology, 17 papers in Physiology and 16 papers in Cellular and Molecular Neuroscience. Recurrent topics in Benjamin Schmid's work include Pluripotent Stem Cells Research (25 papers), CRISPR and Genetic Engineering (22 papers) and Genetic Neurodegenerative Diseases (8 papers). Benjamin Schmid is often cited by papers focused on Pluripotent Stem Cells Research (25 papers), CRISPR and Genetic Engineering (22 papers) and Genetic Neurodegenerative Diseases (8 papers). Benjamin Schmid collaborates with scholars based in Germany, Denmark and Thailand. Benjamin Schmid's co-authors include Thomas Gasser, Ina Kötter, Lutz Heide, Bjørn Holst, Daniela Berg, Troels T. Nielsen, Kristine Freude, Michela Deleidi, David C. Schöndorf and K. Harzer and has published in prestigious journals such as Nature Communications, Journal of Neuroscience and PLoS ONE.

In The Last Decade

Benjamin Schmid

60 papers receiving 1.9k citations

Hit Papers

iPSC-derived neurons from GBA1-associated Parkinson’s dis... 2014 2026 2018 2022 2014 100 200 300 400
What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

  1. iPSC-derived neurons from GBA1-associated Parkinson’s disease patients show autophagic defects and impaired calcium homeostasis
    2014 406 citations David C. Schöndorf, Benjamin Schmid et al. profile →

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Benjamin Schmid Germany 22 991 551 412 389 228 60 1.9k
Li Feng United States 24 735 0.7× 406 0.7× 300 0.7× 411 1.1× 212 0.9× 66 1.8k
Neelam Shahani United States 26 1.5k 1.5× 588 1.1× 385 0.9× 696 1.8× 262 1.1× 39 2.6k
Roberto Di Maio United States 19 796 0.8× 365 0.7× 752 1.8× 641 1.6× 183 0.8× 35 1.8k
Cécile Brocard Austria 26 1.8k 1.8× 342 0.6× 159 0.4× 547 1.4× 225 1.0× 61 2.5k
Ross Bland New Zealand 18 1.4k 1.4× 406 0.7× 431 1.0× 1.1k 2.8× 98 0.4× 30 2.8k
Jin H. Son United States 26 1.1k 1.1× 327 0.6× 497 1.2× 751 1.9× 207 0.9× 60 2.4k
Natalija Popović Spain 24 1.1k 1.1× 564 1.0× 350 0.8× 1.0k 2.6× 86 0.4× 54 2.4k
Madepalli K. Lakshmana United States 25 706 0.7× 529 1.0× 132 0.3× 327 0.8× 206 0.9× 74 1.7k
Linghui Zeng China 28 1.3k 1.3× 460 0.8× 120 0.3× 785 2.0× 155 0.7× 103 2.7k
Hyemyung Seo South Korea 35 1.9k 1.9× 621 1.1× 572 1.4× 1.2k 3.1× 363 1.6× 70 3.4k

Countries citing papers authored by Benjamin Schmid

Since Specialization
Citations

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

Fields of papers citing papers by Benjamin Schmid

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Benjamin Schmid

This figure shows the co-authorship network connecting the top 25 collaborators of Benjamin Schmid. A scholar is included among the top collaborators of Benjamin Schmid 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 Benjamin Schmid. Benjamin Schmid 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.
Rasmussen, Izabela, Niels H. Skotte, Costanza Ferrari Bardile, et al.. (2025). A potential role for NADPH oxidase (NOX1/2) in mutant huntingtin-induced anomalous neurite outgrowth. Molecular and Cellular Neuroscience. 134. 104012–104012. 1 indexed citations
2.
Kettenhofen, Ralf, Benjamin Schmid, Christian Clausen, et al.. (2023). Production of Human Neurogenin 2-Inducible Neurons in a Three-Dimensional Suspension Bioreactor. Journal of Visualized Experiments. 1 indexed citations
3.
Schmid, Benjamin, Mikkel A. Rasmussen, Christian Clausen, et al.. (2019). Generation of a set of isogenic, gene-edited iPSC lines homozygous for all main APOE variants and an APOE knock-out line. Stem Cell Research. 34. 101349–101349. 32 indexed citations
4.
Holst, Bjørn, et al.. (2019). Generation of two isogenic iPSC lines with either a heterozygous or a homozygous E280A mutation in the PSEN1 gene. Stem Cell Research. 35. 101403–101403. 18 indexed citations
5.
Holst, Bjørn, et al.. (2018). Generation of two iPSC lines with either a heterozygous V717I or a heterozygous KM670/671NL mutation in the APP gene. Stem Cell Research. 34. 101368–101368. 14 indexed citations
6.
Marrone, Lara, David C. Schöndorf, Julia C. Fitzgerald, et al.. (2018). Generation of iPSCs carrying a common LRRK2 risk allele for in vitro modeling of idiopathic Parkinson's disease. PLoS ONE. 13(3). e0192497–e0192497. 21 indexed citations
7.
Rasmussen, Mikkel A., Christian Clausen, Ulrike A. Mau‐Holzmann, et al.. (2016). Generation of induced pluripotent stem cells derived from a 77-year-old healthy woman as control for age related diseases. Stem Cell Research. 17(3). 550–552. 2 indexed citations
8.
Rasmussen, Mikkel A., Christian Clausen, Ulrike A. Mau‐Holzmann, et al.. (2016). Generation of an isogenic, gene-corrected iPSC line from a symptomatic 59-year-old female patient with frontotemporal dementia caused by an R406W mutation in the microtubule associated protein tau (MAPT) gene. Stem Cell Research. 17(3). 576–579. 10 indexed citations
9.
Zhang, Yu, Benjamin Schmid, Troels T. Nielsen, et al.. (2016). Generation of a human induced pluripotent stem cell line via CRISPR-Cas9 mediated integration of a site-specific heterozygous mutation in CHMP2B. Stem Cell Research. 17(1). 148–150. 7 indexed citations
10.
Zhang, Yu, Benjamin Schmid, Troels T. Nielsen, et al.. (2016). Generation of a human induced pluripotent stem cell line via CRISPR-Cas9 mediated integration of a site-specific homozygous mutation in CHMP2B. Stem Cell Research. 17(1). 151–153. 5 indexed citations
11.
Kitiyanant, Narisorn, Mikkel A. Rasmussen, Christian Clausen, et al.. (2016). Generation of an isogenic, gene-corrected iPSC line from a symptomatic 57-year-old female patient with frontotemporal dementia caused by a P301L mutation in the microtubule associated protein tau (MAPT) gene. Stem Cell Research. 17(3). 556–559. 12 indexed citations
12.
Rasmussen, Mikkel A., Christian Clausen, Ulrike A. Mau‐Holzmann, et al.. (2016). Generation of an isogenic, gene-corrected iPSC line from a pre-symptomatic 28-year-old woman with an R406W mutation in the microtubule associated protein tau (MAPT) gene. Stem Cell Research. 17(3). 600–602. 4 indexed citations
13.
Schmid, Benjamin, Alisa Tubsuwan, Ulrike A. Mau‐Holzmann, et al.. (2016). Generation of an isogenic, gene-corrected control cell line of the spinocerebellar ataxia type 2 patient-derived iPSC line H271. Stem Cell Research. 16(1). 180–183. 18 indexed citations
14.
Rasmussen, Mikkel A., Christian Clausen, Ulrike A. Mau‐Holzmann, et al.. (2016). Induced pluripotent stem cells (iPSCs) derived from a symptomatic carrier of a S305I mutation in the microtubule-associated protein tau (MAPT)-gene causing frontotemporal dementia. Stem Cell Research. 17(3). 564–567. 3 indexed citations
15.
Tubsuwan, Alisa, Benjamin Schmid, Ulrike A. Mau‐Holzmann, et al.. (2016). Generation of an isogenic, gene-corrected control cell line of the spinocerebellar ataxia type 2 patient-derived iPSC line H266. Stem Cell Research. 16(1). 202–205. 17 indexed citations
16.
Tubsuwan, Alisa, Benjamin Schmid, Poul Hyttel, et al.. (2016). Generation of spinocerebellar ataxia type 2 patient-derived iPSC line H271. Stem Cell Research. 16(1). 159–161. 6 indexed citations
17.
Tubsuwan, Alisa, Mikkel A. Rasmussen, Benjamin Schmid, et al.. (2015). Generation of induced pluripotent stem cells (iPSCs) from an Alzheimer's disease patient carrying a L150P mutation in PSEN-1. Stem Cell Research. 16(1). 110–112. 19 indexed citations
18.
Habisch, Hansjörg, Benjamin Schmid, Christine A. F. Von Arnim, et al.. (2009). Efficient Processing of Alzheimer's Disease Amyloid-Beta Peptides by Neuroectodermally Converted Mesenchymal Stem Cells. Stem Cells and Development. 19(5). 629–633. 17 indexed citations
19.
20.
Schmid, Benjamin, Barbara C. Paton, Konrad Sandhoff, & K. Harzer. (1992). Metabolism of GM1 ganglioside in cultured skin fibroblasts: anomalies in gangliosidoses, sialidoses, and sphingolipid activator protein (SAP, saposin) 1 and prosaposin deficient disorders. Human Genetics. 89(5). 513–8. 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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