Samuel E. Marsh

5.9k total citations · 1 hit paper
13 papers, 2.5k citations indexed

About

Samuel E. Marsh is a scholar working on Neurology, Physiology and Immunology. According to data from OpenAlex, Samuel E. Marsh has authored 13 papers receiving a total of 2.5k indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Neurology, 7 papers in Physiology and 4 papers in Immunology. Recurrent topics in Samuel E. Marsh's work include Neuroinflammation and Neurodegeneration Mechanisms (8 papers), Alzheimer's disease research and treatments (7 papers) and Tryptophan and brain disorders (3 papers). Samuel E. Marsh is often cited by papers focused on Neuroinflammation and Neurodegeneration Mechanisms (8 papers), Alzheimer's disease research and treatments (7 papers) and Tryptophan and brain disorders (3 papers). Samuel E. Marsh collaborates with scholars based in United States, Switzerland and Sweden. Samuel E. Marsh's co-authors include Beth Stevens, Mathew Blurton‐Jones, Timothy R. Hammond, Alec Wysoker, Jinmiao Chen, Steven A. McCarroll, Adam M. H. Young, James Nemesh, Stefanie Giera and Connor Dufort and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Neuron and Immunity.

In The Last Decade

Samuel E. Marsh

12 papers receiving 2.5k citations

Hit Papers

Single-Cell RNA Sequencing of Microglia throughout the Mo... 2018 2026 2020 2023 2018 400 800 1.2k
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. Single-Cell RNA Sequencing of Microglia throughout the Mouse Lifespan and in the Injured Brain Reveals Complex Cell-State Changes
    2018 1.4k citations Timothy R. Hammond, Connor Dufort et al. Immunity profile →

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Samuel E. Marsh United States 11 1.7k 909 715 643 372 13 2.5k
Rachel Rice United States 8 1.9k 1.1× 868 1.0× 428 0.6× 554 0.9× 409 1.1× 22 2.4k
Elizabeth E. Spangenberg United States 9 2.4k 1.4× 1.0k 1.1× 688 1.0× 909 1.4× 578 1.6× 9 3.3k
Chotima Böttcher Germany 18 2.1k 1.2× 1.2k 1.4× 700 1.0× 396 0.6× 271 0.7× 40 2.8k
Allison R. Najafi United States 11 2.5k 1.5× 1.1k 1.2× 425 0.6× 744 1.2× 501 1.3× 12 3.1k
Inge R. Holtman Netherlands 21 2.6k 1.5× 1.6k 1.8× 906 1.3× 806 1.3× 386 1.0× 34 3.7k
Saranya Ramakrishnan United States 5 1.5k 0.9× 531 0.6× 524 0.7× 964 1.5× 431 1.2× 8 2.3k
Arnaud Frouin United States 4 1.9k 1.1× 668 0.7× 760 1.1× 1.1k 1.7× 826 2.2× 4 2.9k
Alicia A. Babcock Denmark 20 1.5k 0.9× 869 1.0× 483 0.7× 435 0.7× 329 0.9× 30 2.2k
Gennady Landa United States 19 1.5k 0.9× 588 0.6× 438 0.6× 403 0.6× 410 1.1× 41 2.8k
Renzo Mancuso Spain 25 1.4k 0.8× 591 0.7× 1.1k 1.5× 956 1.5× 537 1.4× 50 3.0k

Countries citing papers authored by Samuel E. Marsh

Since Specialization
Citations

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

Fields of papers citing papers by Samuel E. Marsh

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Samuel E. Marsh

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

All Works

13 of 13 papers shown
1.
Qureshi, Yasir H., Diego E. Berman, Samuel E. Marsh, et al.. (2022). The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease. Cell Reports. 38(3). 110262–110262. 19 indexed citations
2.
Marsh, Samuel E., Sarah Louise Murphy, Tushar Kamath, et al.. (2022). Multi‐modal Analysis and Modeling of Human Neurodegenerative Disease to Reveal Disease Mechanisms and Biomarkers. Alzheimer s & Dementia. 18(S4).
3.
Liddelow, Shane A., Samuel E. Marsh, & Beth Stevens. (2020). Microglia and Astrocytes in Disease: Dynamic Duo or Partners in Crime?. Trends in Immunology. 41(9). 820–835. 164 indexed citations
4.
Hammond, Timothy R., Samuel E. Marsh, & Beth Stevens. (2019). Immune Signaling in Neurodegeneration. Immunity. 50(4). 955–974. 236 indexed citations
5.
Hammond, Timothy R., Connor Dufort, Lasse Dissing‐Olesen, et al.. (2018). Single-Cell RNA Sequencing of Microglia throughout the Mouse Lifespan and in the Injured Brain Reveals Complex Cell-State Changes. Immunity. 50(1). 253–271.e6. 1359 indexed citations breakdown →
6.
McIntyre, Laura L., Samuel E. Marsh, Christine A. Schneider, et al.. (2018). CD11a expression distinguishes infiltrating myeloid cells from plaque‐associated microglia in Alzheimer's disease. Glia. 67(5). 844–856. 38 indexed citations
7.
Mathur, Vidhu, Ritwik Burai, Ryan T. Vest, et al.. (2017). Activation of the STING-Dependent Type I Interferon Response Reduces Microglial Reactivity and Neuroinflammation. Neuron. 96(6). 1290–1302.e6. 129 indexed citations
8.
Marsh, Samuel E., Stephen T. Yeung, M.D. Martínez del Valle Torres, et al.. (2017). HuCNS-SC Human NSCs Fail to Differentiate, Form Ectopic Clusters, and Provide No Cognitive Benefits in a Transgenic Model of Alzheimer's Disease. Stem Cell Reports. 8(2). 235–248. 46 indexed citations
9.
Marsh, Samuel E. & Mathew Blurton‐Jones. (2017). Neural stem cell therapy for neurodegenerative disorders: The role of neurotrophic support. Neurochemistry International. 106. 94–100. 136 indexed citations
10.
Goldberg, Natalie R.S., Samuel E. Marsh, Joseph Ochaba, et al.. (2017). Human Neural Progenitor Transplantation Rescues Behavior and Reduces α-Synuclein in a Transgenic Model of Dementia with Lewy Bodies. Stem Cells Translational Medicine. 6(6). 1477–1490. 13 indexed citations
11.
White, André O., et al.. (2017). Front and Back Flipping for Neurobiology! Developing a Hybrid Upper-Division Lab Course.. PubMed. 16(1). A95–A101. 1 indexed citations
12.
Marsh, Samuel E., Edsel M. Abud, Anita Lakatos, et al.. (2016). The adaptive immune system restrains Alzheimer’s disease pathogenesis by modulating microglial function. Proceedings of the National Academy of Sciences. 113(9). E1316–25. 303 indexed citations
13.
Marsh, Samuel E. & Mathew Blurton‐Jones. (2012). Examining the mechanisms that link β-amyloid and α-synuclein pathologies. Alzheimer s Research & Therapy. 4(2). 11–11. 93 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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