Emma Deas

5.7k total citations · 3 hit papers
27 papers, 4.5k citations indexed

About

Emma Deas is a scholar working on Neurology, Molecular Biology and Cellular and Molecular Neuroscience. According to data from OpenAlex, Emma Deas has authored 27 papers receiving a total of 4.5k indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Neurology, 12 papers in Molecular Biology and 8 papers in Cellular and Molecular Neuroscience. Recurrent topics in Emma Deas's work include Parkinson's Disease Mechanisms and Treatments (16 papers), Mitochondrial Function and Pathology (8 papers) and Alzheimer's disease research and treatments (4 papers). Emma Deas is often cited by papers focused on Parkinson's Disease Mechanisms and Treatments (16 papers), Mitochondrial Function and Pathology (8 papers) and Alzheimer's disease research and treatments (4 papers). Emma Deas collaborates with scholars based in United Kingdom, United States and Italy. Emma Deas's co-authors include Nicholas Wood, Hélène Plun‐Favreau, Andrey Y. Abramov, Sonia Gandhi, Victoria L. Harvey, David Klenerman, Nunilo Cremades, Christopher M. Dobson, L. Miguel Martins and Tuomas P. J. Knowles and has published in prestigious journals such as Cell, Proceedings of the National Academy of Sciences and PLoS ONE.

In The Last Decade

Emma Deas

26 papers receiving 4.4k citations

Hit Papers

align trajectories

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.

Direct Observation of the Interconversion of Normal and Toxic Forms of α-Synuclein

2012 709 citations Nunilo Cremades, Samuel I. A. Cohen et al. Cell profile →
Glucocerebrosidase mutations in clinical and pathologically proven Parkinson's disease

2009 509 citations José Brás, Emma Deas et al. Brain profile →
Structural characterization of toxic oligomers that are kinetically trapped during α-synuclein fibril formation

2015 368 citations Serene W. Chen, Srdja Drakulić et al. Proceedings of the National Academy of Sciences profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Emma Deas United Kingdom	23	2.3k	2.1k	1.6k	942	941	27	4.5k
Kenny K. K. Chung Hong Kong	23	2.2k 0.9×	2.2k 1.0×	1.0k 0.6×	1.5k 1.6×	783 0.8×	35	4.4k
Benjamin Dehay France	36	2.8k 1.2×	1.8k 0.9×	1.5k 1.0×	1.5k 1.6×	1.0k 1.1×	90	5.2k
Matthew E. Gegg United Kingdom	29	1.8k 0.8×	1.5k 0.7×	1.8k 1.1×	561 0.6×	1.3k 1.3×	44	4.0k
Yvette C. Wong United States	23	1.7k 0.7×	2.3k 1.1×	1.2k 0.7×	1.0k 1.1×	1.5k 1.5×	32	4.9k
Miratul M. K. Muqit United Kingdom	34	2.5k 1.1×	3.4k 1.6×	1.2k 0.7×	1.3k 1.4×	2.6k 2.8×	63	6.2k
Joseph R. Mazzulli United States	28	3.0k 1.3×	1.8k 0.9×	2.5k 1.5×	1.5k 1.5×	1.1k 1.2×	46	5.7k
Hélène Plun‐Favreau United Kingdom	29	1.6k 0.7×	2.0k 1.0×	798 0.5×	814 0.9×	1.1k 1.2×	44	3.9k
Charbel Moussa United States	36	1.5k 0.6×	1.5k 0.7×	1.6k 1.0×	1.0k 1.1×	793 0.8×	83	4.2k
Wen-Lang Lin United States	36	3.4k 1.5×	2.4k 1.1×	2.2k 1.3×	1.1k 1.1×	374 0.4×	51	5.6k
Jordi Magrané United States	27	1.4k 0.6×	2.2k 1.0×	1.0k 0.6×	781 0.8×	1.1k 1.2×	36	3.9k

Countries citing papers authored by Emma Deas

Since Specialization

Citations

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

Fields of papers citing papers by Emma Deas

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Emma Deas

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

All Works

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20 of 20 papers shown

Chen, Serene W., Srdja Drakulić, Emma Deas, et al.. (2015). Structural characterization of toxic oligomers that are kinetically trapped during α-synuclein fibril formation. Proceedings of the National Academy of Sciences. 112(16). E1994–2003. 368 indexed citations breakdown →

Tufi, Roberta, Sonia Gandhi, Inês Pimenta de Castro, et al.. (2014). Enhancing nucleotide metabolism protects against mitochondrial dysfunction and neurodegeneration in a PINK1 model of Parkinson’s disease. Nature Cell Biology. 16(2). 157–166. 116 indexed citations

Yellon, Derek M., Sang‐Bing Ong, Uma Mukherjee, et al.. (2013). Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury. PLoS ONE. 8(4). e62400–e62400. 109 indexed citations

Yellon, Derek M., Sang‐Bing Ong, Uma Mukherjee, et al.. (2013). Correction: Loss of PINK1 Increases the Heart's Vulnerability to Ischemia-Reperfusion Injury. PLoS ONE. 8(6). 29 indexed citations

Durán, Raquel, Niccolò E. Mencacci, Maryam Shoai, et al.. (2012). The glucocerobrosidase E326K variant predisposes to Parkinson's disease, but does not cause Gaucher's disease. Movement Disorders. 28(2). 232–236. 102 indexed citations

Cremades, Nunilo, Samuel I. A. Cohen, Emma Deas, et al.. (2012). Direct Observation of the Interconversion of Normal and Toxic Forms of α-Synuclein. Cell. 149(5). 1048–1059. 709 indexed citations breakdown →

Wood‐Kaczmar, Alison, Emma Deas, Nicholas Wood, & Andrey Y. Abramov. (2012). The Role of the Mitochondrial NCX in the Mechanism of Neurodegeneration in Parkinson’s Disease. Advances in experimental medicine and biology. 961. 241–249. 25 indexed citations

Plun‐Favreau, Hélène, Victoria Burchell, Kira M. Holmström, et al.. (2012). HtrA2 deficiency causes mitochondrial uncoupling through the F1F0-ATP synthase and consequent ATP depletion. Cell Death and Disease. 3(6). e335–e335. 31 indexed citations

Castro, Inês Pimenta de, David Lam, Roberta Tufi, et al.. (2012). Genetic analysis of mitochondrial protein misfolding in Drosophila melanogaster. Cell Death and Differentiation. 19(8). 1308–1316. 96 indexed citations

10.

Burchell, Victoria, Sonia Gandhi, Emma Deas, et al.. (2010). Targeting mitochondrial dysfunction in neurodegenerative disease: Part II. Expert Opinion on Therapeutic Targets. 14(5). 497–511. 68 indexed citations

11.

Deas, Emma, Hélène Plun‐Favreau, Sonia Gandhi, et al.. (2010). PINK1 cleavage at position A103 by the mitochondrial protease PARL. Human Molecular Genetics. 20(5). 867–879. 390 indexed citations

12.

Burchell, Victoria, Sonia Gandhi, Emma Deas, et al.. (2010). Targeting mitochondrial dysfunction in neurodegenerative disease: Part I. Expert Opinion on Therapeutic Targets. 14(4). 369–385. 52 indexed citations

13.

Brás, José, Emma Deas, Sean S. O’Sullivan, et al.. (2009). Glucocerebrosidase mutations in clinical and pathologically proven Parkinson's disease. Brain. 132(7). 1783–1794. 509 indexed citations breakdown →

14.

Wood‐Kaczmar, Alison, Sonia Gandhi, Zhi Yao, et al.. (2008). PINK1 Is Necessary for Long Term Survival and Mitochondrial Function in Human Dopaminergic Neurons. PLoS ONE. 3(6). e2455–e2455. 258 indexed citations

15.

Plun‐Favreau, Hélène, Sonia Gandhi, Alison Wood‐Kaczmar, et al.. (2008). What Have PINK1 and HtrA2 Genes Told Us about the Role of Mitochondria in Parkinson's Disease?. Annals of the New York Academy of Sciences. 1147(1). 30–36. 17 indexed citations

16.

Kalscheuer, Vera M., Luciana Musante, Cheng Fang, et al.. (2008). A balanced chromosomal translocation disruptingARHGEF9is associated with epilepsy, anxiety, aggression, and mental retardation. Human Mutation. 30(1). 61–68. 120 indexed citations

17.

Plun‐Favreau, Hélène, Kristina Klupsch, Nicoleta Moisoi, et al.. (2007). The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1. Nature Cell Biology. 9(11). 1243–1252. 383 indexed citations

18.

Abou‐Sleiman, Patrick M., Miratul M. K. Muqit, Neil Q. McDonald, et al.. (2006). A heterozygous effect for PINK1 mutations in Parkinson's disease?. Annals of Neurology. 60(4). 414–419. 131 indexed citations

19.

Muqit, Miratul M. K., Patrick M. Abou‐Sleiman, Adrian T. Saurin, et al.. (2006). Altered cleavage and localization of PINK1 to aggresomes in the presence of proteasomal stress. Journal of Neurochemistry. 98(1). 156–169. 138 indexed citations

20.

Ditzel, Mark, Rebecca Wilson, Tencho Tenev, et al.. (2003). Degradation of DIAP1 by the N-end rule pathway is essential for regulating apoptosis. Nature Cell Biology. 5(5). 467–473. 190 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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