Colúm Connolly

665 total citations
9 papers, 316 citations indexed

About

Colúm Connolly is a scholar working on Cellular and Molecular Neuroscience, Molecular Biology and Neurology. According to data from OpenAlex, Colúm Connolly has authored 9 papers receiving a total of 316 indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Cellular and Molecular Neuroscience, 5 papers in Molecular Biology and 5 papers in Neurology. Recurrent topics in Colúm Connolly's work include Genetic Neurodegenerative Diseases (6 papers), Neuroinflammation and Neurodegeneration Mechanisms (5 papers) and Mitochondrial Function and Pathology (2 papers). Colúm Connolly is often cited by papers focused on Genetic Neurodegenerative Diseases (6 papers), Neuroinflammation and Neurodegeneration Mechanisms (5 papers) and Mitochondrial Function and Pathology (2 papers). Colúm Connolly collaborates with scholars based in Canada, Sweden and Switzerland. Colúm Connolly's co-authors include Blair R. Leavitt, Austin Hill, Michael R. Hayden, Jae Kyu Ryu, James G. McLarnon, Sonia Franciosi, Terri L. Petkau, Maria Björkqvist, Eliezer Masliah and Kristina Bečanović and has published in prestigious journals such as Neuroscience, Human Molecular Genetics and Neurobiology of Disease.

In The Last Decade

Colúm Connolly

9 papers receiving 312 citations

Peers

Colúm Connolly

MB

CMN

NEURO

PHYSI

S. Sebastian Pineda United States

Hélèna L. Denis Canada

Galina Marsh United States

Andrea Wetzel United Kingdom

Rasmus Rydbirk Denmark

Kamil Grzyb Luxembourg

Misako Kunii Japan

Michel Meijer Netherlands

Bradford Casey United States

Lina Issa Germany

S. Sebastian Pineda United States

Colúm Connolly

221 ×1.2

MB

147 ×0.9

CMN

61 ×0.7

NEURO

73 ×0.9

NEURO

47 ×0.9

PHYSI

Citations per year, relative to Colúm Connolly Colúm Connolly (= 1×) peers S. Sebastian Pineda

Countries citing papers authored by Colúm Connolly

Since Specialization

Citations

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

Fields of papers citing papers by Colúm Connolly

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Colúm Connolly

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

All Works

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9 of 9 papers shown

1.

Connolly, Colúm, et al.. (2025). Emerging roles of microglia and neuroinflammation in Huntington's disease: From pathophysiology to clinical trials. Journal of Huntington s Disease. 14(3). 241–257. 2 indexed citations

2.

Petkau, Terri L., et al.. (2019). Isolating cells from adult murine brain for validation of cell-type specific cre-mediated deletion. Journal of Neuroscience Methods. 328. 108422–108422. 1 indexed citations

3.

Petkau, Terri L., et al.. (2019). Mutant huntingtin expression in microglia is neither required nor sufficient to cause the Huntington’s disease-like phenotype in BACHD mice. Human Molecular Genetics. 28(10). 1661–1670. 28 indexed citations

4.

Petkau, Terri L., et al.. (2017). Selective depletion of microglial progranulin in mice is not sufficient to cause neuronal ceroid lipofuscinosis or neuroinflammation. Journal of Neuroinflammation. 14(1). 225–225. 29 indexed citations

5.

Connolly, Colúm, Guihua Lu, Amber L. Southwell, et al.. (2016). Enhanced immune response to MMP3 stimulation in microglia expressing mutant huntingtin. Neuroscience. 325. 74–88. 34 indexed citations

6.

Jan, Asad, Joanna M. Karasinska, Martin H. Kang, et al.. (2015). Direct intracerebral delivery of a miR-33 antisense oligonucelotide into mouse brain increases brain ABCA1 expression. Neuroscience Letters. 598. 66–72. 24 indexed citations

7.

Träger, Ulrike, Ralph André, James R. C. Miller, et al.. (2014). Characterisation of immune cell function in fragment and full-length Huntington's disease mouse models. Neurobiology of Disease. 73. 388–398. 52 indexed citations

8.

Tang, Bin, Kristina Bečanović, Paula Desplats, et al.. (2012). Forkhead box protein p1 is a transcriptional repressor of immune signaling in the CNS: implications for transcriptional dysregulation in Huntington disease. Human Molecular Genetics. 21(14). 3097–3111. 43 indexed citations

9.

Franciosi, Sonia, Jae Kyu Ryu, Austin Hill, et al.. (2011). Age-dependent neurovascular abnormalities and altered microglial morphology in the YAC128 mouse model of Huntington disease. Neurobiology of Disease. 45(1). 438–449. 103 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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