A collaborative study of genetic linkage of bipolar manic‐depressive illness and red/green colorblindness : A PROJECT OF THE BIOLOGICAL PSYCHIATRY COLLABORATIVE PROGRAM OF THE WORLD HEALTH ORGANIZATION

Gershon, Elliot S.; Mendlewicz, J.; Gastpar, Markus; Bech, Per; Goldin, Lynn R.; Kielholz, P; Rafaelsen, O. J.; Vartanian, Felix; Bunney, William E.

doi:10.1111/j.1600-0447.1980.tb00585.x

Cited by 46 publications

(1 citation statement)

References 14 publications

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“…The finding was supported by evidence for linkage between manic-depressive illness and color blindness (protanopia and deuteranopia) (Xq28) [Baron, 1977;Mendlewicz et al, 1979], although the evidence for linkage was not universal [Gershon et al, 1979[Gershon et al, , 1980. Eventually glucose-6-phosphate dehydrogenase (G6PD), a biochemical marker encoded by a gene on Xq28, was subjected to linkage studies and revealed a lod score of 4.32 in a large family of Persian Sephardic Jewish origin segregating both BD and G6PD deficiency .…”

Section: Bd and X Chromosomementioning

confidence: 73%

Epigenetics and bipolar disorder: New opportunities and challenges

Petronis

2003

American J of Med Genetics Pt C

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Despite significant effort, understanding of the molecular causes and mechanisms of bipolar disorder (BD) remains a major challenge. Numerous molecular genetic linkage and association studies have been conducted over the last two decades; however, the data are quite inconsistent or even controversial. This article develops an argument that molecular studies of BD would benefit significantly from adding an epigenetic (epiG) perspective. EpiG factors refer to modifications of DNA and chromatin that "orchestrate" the activity of the genome, including regulation of gene expression. EpiG mechanisms are consistent with various non-Mendelian features of BD such as the relatively high degree of discordance in monozygotic (MZ) twins, the critical age group for susceptibility to the disease, clinical differences in males and females, and fluctuation of the disease course, including interchanges of manic and depressive phases, among others. Apart from the phenomenological consistency, molecular epiG peculiarities may shed new light on the understanding of controversial molecular genetic findings. The relevance of epigenetics for the molecular studies of BD is demonstrated using the examples of genetic studies of BD on chromosome 11p and the X chromosome. A spectrum of epiG mechanisms such as genomic imprinting, tissue-specific effects, paramutagenesis, and epiG polymorphism, as well as epiG regulation of X chromosome inactivation, is introduced. All this serves the goal of demonstrating that epiG factors cannot be ignored anymore in complex phenotypes such as BD, and systematic large-scale epiG studies of BD have to be initiated.

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Section: Bd and X Chromosomementioning

confidence: 73%