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DNA methylation in a Scottish family multiply affected by bipolar disorder and major depressive disorder

Overview of attention for article published in Clinical Epigenetics, January 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (82nd percentile)
  • Good Attention Score compared to outputs of the same age and source (73rd percentile)

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Title
DNA methylation in a Scottish family multiply affected by bipolar disorder and major depressive disorder
Published in
Clinical Epigenetics, January 2016
DOI 10.1186/s13148-016-0171-z
Pubmed ID
Authors

Rosie May Walker, Andrea Nikie Christoforou, Daniel L. McCartney, Stewart W. Morris, Nicholas A. Kennedy, Peter Morten, Susan Maguire Anderson, Helen Scott Torrance, Alix Macdonald, Jessika Elizabeth Sussmann, Heather Clare Whalley, Douglas H. R. Blackwood, Andrew Mark McIntosh, David John Porteous, Kathryn Louise Evans

Abstract

Bipolar disorder (BD) is a severe, familial psychiatric condition. Progress in understanding the aetiology of BD has been hampered by substantial phenotypic and genetic heterogeneity. We sought to mitigate these confounders by studying a multi-generational family multiply affected by BD and major depressive disorder (MDD), who carry an illness-linked haplotype on chromosome 4p. Within a family, aetiological heterogeneity is likely to be reduced, thus conferring greater power to detect illness-related changes. As accumulating evidence suggests that altered DNA methylation confers risk for BD and MDD, we compared genome-wide methylation between (i) affected carriers of the linked haplotype (ALH) and married-in controls (MIs), (ii) well unaffected haplotype carriers (ULH) and MI, (iii) ALH and ULH and (iv) all haplotype carriers (LH) and MI. Nominally significant differences in DNA methylation were observed in all comparisons, with differences withstanding correction for multiple testing when the ALH or LH group was compared to the MIs. In both comparisons, we observed increased methylation at a locus in FANCI, which was accompanied by increased FANCI expression in the ALH group. FANCI is part of the Fanconi anaemia complementation (FANC) gene family, which are mutated in Fanconi anaemia and participate in DNA repair. Interestingly, several FANC genes have been implicated in psychiatric disorders. Regional analyses of methylation differences identified loci implicated in psychiatric illness by genome-wide association studies, including CACNB2 and the major histocompatibility complex. Gene ontology analysis revealed enrichment for methylation differences in neurologically relevant genes. Our results highlight altered DNA methylation as a potential mechanism by which the linked haplotype might confer risk for mood disorders. Differences in the phenotypic outcome of haplotype carriers might, in part, arise from additional changes in DNA methylation that converge on neurologically important pathways. Further work is required to investigate the underlying mechanisms and functional consequences of the observed differences in methylation.

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X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 69 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 1%
United States 1 1%
Unknown 67 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 14 20%
Student > Master 7 10%
Student > Bachelor 6 9%
Researcher 5 7%
Student > Postgraduate 4 6%
Other 17 25%
Unknown 16 23%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 12 17%
Agricultural and Biological Sciences 6 9%
Medicine and Dentistry 6 9%
Psychology 6 9%
Neuroscience 5 7%
Other 14 20%
Unknown 20 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 8. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 February 2016.
All research outputs
#4,099,243
of 23,341,064 outputs
Outputs from Clinical Epigenetics
#274
of 1,291 outputs
Outputs of similar age
#70,538
of 397,271 outputs
Outputs of similar age from Clinical Epigenetics
#14
of 53 outputs
Altmetric has tracked 23,341,064 research outputs across all sources so far. Compared to these this one has done well and is in the 82nd percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,291 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.1. This one has done well, scoring higher than 78% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 397,271 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 82% of its contemporaries.
We're also able to compare this research output to 53 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 73% of its contemporaries.