No genetic support for a contribution of prostaglandins to the aetiology of androgenetic alopecia
| Autor: | Heilmann, S., Nyholt, D. R., Bataille, V., Brockschmidt, F. F., Dedoussis, G., Deloukas, P., den Heijer, M., Dimitriou, M., Eigelshoven, S., Eriksson, N., Geller, F., Glass, D., Hanneken, S., Heath, A. C., Hillmer, A. M., Hinds, D. A., Kanoni, S., Kárason, A., Kiefer, A. K., Kiemeney, L. A., Li, R., Mangino, M., Martin, N. G., Medland, S. E., Moebus, S., Montgomery, G. W., Mooser, V., Richards, J. B., Song, K., Spector, T. D., Herold, C., Stefansson, H., Stefansson, K., Sulem, P., Tung, J. Y., Vermeulen, S. H., Vollenweider, P., Waterworth, D., Consortium, Maan, Becker, T., Nöthen, M. M., Consortium, Meta-Analysis for Androgenetic Alopecia Novel Determinants |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Candidate gene
Receptors Prostaglandin Genome-wide association study Aetiology screening and detection [ONCOL 5] Dermatology Disease Biology Molecular epidemiology [NCEBP 1] Genetic predisposition medicine genetics [Receptors Immunologic] Humans ddc:610 Receptors Immunologic genetics [Alopecia] Molecular epidemiology Aetiology screening and detection [NCEBP 1] Genetic association genetics [Prostaglandin D2] Genetics Prostaglandin D2 Alopecia medicine.disease Phenotype genetics [Receptors Prostaglandin] Hair loss metabolism [Prostaglandin D2] Trait prostaglandin D2 receptor |
| Zdroj: | British Journal of Dermatology, 169, 222-4 British Journal of Dermatology, 169, 1, pp. 222-4 British journal of dermatology 169(1), 222-224 (2013). doi:10.1111/bjd.12292 |
| ISSN: | 0007-0963 |
| Popis: | MADAM, Androgenetic alopecia (AGA) is a common age-dependent trait, characterized by a progressive loss of hair from the scalp. The hair loss may commence during puberty and up to 80% of white men experience some degree of AGA during their lifetime.1 Research has established that two essential aetiological factors for AGA are a genetic predisposition and the presence of androgens (male sex hormones).1,2 A recent meta-analysis of genome-wide association studies (GWAS) has increased the number of identified loci associated with this trait at the molecular level to a total of eight.3 However, despite these successes, a large fraction of the genetic contribution remains to be identified. One way to identify further genetic loci is to combine the resource of GWAS datasets with knowledge about specific biological factors likely to be involved in the development of disease. The focused evaluation of a limited number of candidate genes in GWAS datasets avoids the necessity for extensive correction for multiple testing, which typically limits the power for detecting genetic loci at a genome-wide level.4 Because the presence of genetic association suggests that candidate genes are likely to operate early in the causative chain of events leading to the phenotype, this approach may also function to favour biological pathways for their importance in the development of AGA. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text