John Collinge

28.4k total citations · 3 hit papers
36 papers, 4.3k citations indexed

About

John Collinge is a scholar working on Molecular Biology, Physiology and Neurology. According to data from OpenAlex, John Collinge has authored 36 papers receiving a total of 4.3k indexed citations (citations by other indexed papers that have themselves been cited), including 21 papers in Molecular Biology, 21 papers in Physiology and 11 papers in Neurology. Recurrent topics in John Collinge's work include Alzheimer's disease research and treatments (18 papers), Prion Diseases and Protein Misfolding (13 papers) and Neurological diseases and metabolism (10 papers). John Collinge is often cited by papers focused on Alzheimer's disease research and treatments (18 papers), Prion Diseases and Protein Misfolding (13 papers) and Neurological diseases and metabolism (10 papers). John Collinge collaborates with scholars based in United Kingdom, United States and Denmark. John Collinge's co-authors include Martin N. Rossor, Wai‐Ming Yau, Robert Tycko, Elizabeth Fisher, Junxia Lu, Wei Qiang, Corinne J. Smith, Mark S. Palmer, Miles A. Whittington and Anthony R. Clarke and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Nature Communications.

In The Last Decade

John Collinge

36 papers receiving 4.2k 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.

Mutations in the endosomal ESCRTIII-complex subunit CHMP2B in frontotemporal dementia

2005 605 citations Nick Parkinson, Jeremy Brown et al. profile →
Prion protein is necessary for normal synaptic function

1994 595 citations John Collinge, Miles A. Whittington et al. Nature profile →
Structural variation in amyloid-β fibrils from Alzheimer's disease clinical subtypes

2017 497 citations John Collinge et al. Nature profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
John Collinge United Kingdom	29	2.2k	2.1k	1.5k	1.1k	510	36	4.3k
Chris Van den Haute Belgium	45	3.0k 1.4×	2.5k 1.2×	2.3k 1.5×	1.2k 1.0×	2.1k 4.2×	120	7.1k
Anna Stieber United States	34	2.7k 1.2×	2.9k 1.4×	3.4k 2.3×	1.5k 1.3×	1.7k 3.4×	80	6.9k
Karin M. Danzer Germany	30	2.0k 0.9×	1.5k 0.7×	2.9k 1.9×	1.0k 0.9×	1.1k 2.3×	61	4.7k
H. A. Kretzschmar Germany	41	4.2k 1.9×	1.1k 0.5×	1.3k 0.9×	2.1k 1.9×	315 0.6×	99	5.6k
Giovanna R. Mallucci United Kingdom	32	3.6k 1.6×	1.4k 0.7×	669 0.4×	1.3k 1.1×	797 1.6×	55	5.4k
Athena Andreadis United States	36	3.8k 1.7×	3.2k 1.5×	1.5k 1.0×	967 0.8×	1.5k 3.0×	57	6.4k
Manu Sharma United States	25	2.0k 0.9×	1.6k 0.8×	2.5k 1.6×	515 0.4×	1.5k 2.9×	36	5.5k
Laura A. Volpicelli‐Daley United States	42	2.3k 1.0×	2.0k 0.9×	4.3k 2.9×	1.2k 1.0×	2.1k 4.1×	71	6.9k
Takumi Akagi Japan	25	1.6k 0.7×	1.1k 0.5×	396 0.3×	284 0.2×	929 1.8×	45	3.0k
Maria Teresa Ciotti Italy	43	2.1k 0.9×	1.3k 0.6×	266 0.2×	683 0.6×	1.4k 2.8×	129	4.6k

Countries citing papers authored by John Collinge

Since Specialization

Citations

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

Fields of papers citing papers by John Collinge

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of John Collinge

This figure shows the co-authorship network connecting the top 25 collaborators of John Collinge. A scholar is included among the top collaborators of John Collinge 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 John Collinge. John Collinge 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

Rostgaard, Nina, Esben Budtz–Jørgensen, Peter Johannsen, et al.. (2017). TMEM106B and ApoE polymorphisms in CHMP2B-mediated frontotemporal dementia (FTD-3). Neurobiology of Aging. 59. 221.e1–221.e7. 3 indexed citations

Zhang, Dainan, Yingjie Qi, Igor Klyubin, et al.. (2017). Targeting glutamatergic and cellular prion protein mechanisms of amyloid β-mediated persistent synaptic plasticity disruption: Longitudinal studies. Neuropharmacology. 121. 231–246. 23 indexed citations

Hu, Neng‐Wei, Andrew J. Nicoll, Alexandra J. Mably, et al.. (2014). mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo. Nature Communications. 5(1). 3374–3374. 143 indexed citations

Fratta, Pietro, Mark Poulter, Tammaryn Lashley, et al.. (2013). Homozygosity for the C9orf72 GGGGCC repeat expansion in frontotemporal dementia. Acta Neuropathologica. 126(3). 401–409. 104 indexed citations

Ghazi‐Noori, Shabnam, Kristina E. Froud, Sarah Mizielinska, et al.. (2012). Progressive neuronal inclusion formation and axonal degeneration in CHMP2B mutant transgenic mice. Brain. 135(3). 819–832. 80 indexed citations

O’Nuallain, Brian, Darragh B. Freir, Andrew J. Nicoll, et al.. (2010). Amyloid β-Protein Dimers Rapidly Form Stable Synaptotoxic Protofibrils. Journal of Neuroscience. 30(43). 14411–14419. 222 indexed citations

Urwin, Hazel, Jørgen E. Nielsen, Daniel Metcalf, et al.. (2010). Disruption of endocytic trafficking in frontotemporal dementia with CHMP2B mutations. Human Molecular Genetics. 19(11). 2228–2238. 142 indexed citations

Guerreiro, Rita, John S. Beck, J. Raphael Gibbs, et al.. (2010). Genetic Variability in CLU and Its Association with Alzheimer's Disease. PLoS ONE. 5(3). e9510–e9510. 44 indexed citations

Rollinson, Sara, Jonathan D. Rohrer, Julie van der Zee, et al.. (2009). No association of PGRN 3′UTR rs5848 in frontotemporal lobar degeneration. Neurobiology of Aging. 32(4). 754–755. 32 indexed citations

10.

Rohrer, Jonathan D., Jason D. Warren, Rohani Omar, et al.. (2008). Parietal Lobe Deficits in Frontotemporal Lobar Degeneration Caused by a Mutation in the Progranulin Gene. Archives of Neurology. 65(4). 506–506. 42 indexed citations

11.

Beck, Jon, Jonathan D. Rohrer, Adrian M. Isaacs, et al.. (2008). A distinct clinical, neuropsychological and radiological phenotype is associated with progranulin gene mutations in a large UK series. Brain. 131(3). 706–720. 173 indexed citations

12.

Rohrer, Jonathan D., Jason D. Warren, Josephine Barnes, et al.. (2008). Mapping the progression of progranulin-associated frontotemporal lobar degeneration. Nature Clinical Practice Neurology. 4(8). 455–460. 34 indexed citations

13.

Zee, Julie van der, Hazel Urwin, Sebastiaan Engelborghs, et al.. (2007). CHMP2B C-truncating mutations in frontotemporal lobar degeneration are associated with an aberrant endosomal phenotype in vitro. Human Molecular Genetics. 17(2). 313–322. 121 indexed citations

14.

Janssen, John C., Nick C. Fox, Richard Harvey, et al.. (2000). Alzheimer's disease due to an intronic presenilin-1 (PSEN1 intron 4) mutation. Brain. 123(5). 894–907. 26 indexed citations

15.

Mead, Simon, Jonathan Beck, Andrew Dickinson, Elizabeth Fisher, & John Collinge. (2000). Examination of the human prion protein-like gene Doppel for genetic susceptibility to sporadic and variant Creutzfeldt–Jakob disease. Neuroscience Letters. 290(2). 117–120. 49 indexed citations

16.

Lloyd, S. J., Jeremy Brown, Susanne Gydesen, et al.. (1999). Molecular Genetic Characterisation of Frontotemporal Dementia on Chromosome 3. Dementia and Geriatric Cognitive Disorders. 10(Suppl. 1). 93–101. 44 indexed citations

17.

Smith, Corinne J., Alex F. Drake, Graham B. Bloomberg, et al.. (1997). Conformational properties of the prion octa‐repeat and hydrophobic sequences. FEBS Letters. 405(3). 378–384. 36 indexed citations

18.

Basun, Hans, Ove Almkvist, Karin Axelman, et al.. (1997). Clinical Characteristics of a Chromosome 17--Linked Rapidly Progressive Familial Frontotemporal Dementia. Archives of Neurology. 54(5). 539–544. 49 indexed citations

19.

Budka, Herbert, Adriano Aguzzi, Paul Brown, et al.. (1995). Tissue Handling in Suspected Creutzfeldt‐Jakob Disease (CJD) and Other Human Spongiform Encephalopathies (Prion Diseases). Brain Pathology. 5(3). 319–322. 71 indexed citations

20.

Collinge, John, Miles A. Whittington, Katie Sidle, et al.. (1994). Prion protein is necessary for normal synaptic function. Nature. 370(6487). 295–297. 595 indexed citations breakdown →

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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