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1. Six novel susceptibility Loci for early-onset androgenetic alopecia and their unexpected... 2012

   https://ncsu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3db9MwELdYEYgXBAOxwCgGIfGUNa2d2nnsyqpN2kdFNzTxErn-2Cp1SbW0iP733DlJ1aA9TLxYVXyJUt9H7uy73xHyVU1dbB0zoGmRCkFCbJgYw8JprEG_lMOTruZmDonrWhiftK-ns4NsfneQzW59buXiTnfqPLHO-GzIWB_8-qSzQ3YE43WIXppfFsuyo0ocs1BARF_VyzHR7VTsOVgAbzz2qODYwgg8kIRxRCvd-jR5BP-NnW4t5nnxkBP6by7l1sdp9Iq8rLxKOijf_jV5YrNd8qzsM7neJc_PqhP0N2Q9mf2h5_lvO6eTVeFzWnx67JqeApsouLDUYx6HF1lhlxTzHXP4H1jqSAfz3Herpyoz9BJPGOhVhi0CNLitdIvRFHd3KdaewO_v5RFQ8ZZcjY4uh8dh1X4h1H0ZLUOle05Ip5RzPbSCVlipBDhQhoEPaBkTzIhYIR6948LwaGq0dgK1WnEZWbZHqFTcSoh1JeOCJyyRwiRGur6JbKSYigIS1kueLkp4jdSfsQkIS8q1S5FbacWtgBwiXza0CI7tL-T3N2klImnSl13ddV0jNIia4UkUKQibnJbY_kyYgHxCrqZlpelGxdNBL-FMIABRQL54CgTIyDAD50atiiI9ufj5CKLJ-WOIfjSIvlVELgch0qoqjcgzi-hcDcr9BiXYAt2Y3kNBrZeugIXssj5C4OGdtfA-PP15M40PxdS7zOYroIGAIsYK7F5A3pWyvln-WnMCIhpa0OBPcwZ02oOYVzr8_r_v_EBegPPaK5NP90lreb-yH0kLK1_aYBeuhR8P236XBcajyTWMo_Fpmzw9Hp6MfrUxz3fc9tbjL_VHbCM

   Li, Rui; Brockschmidt, Felix F; Kiefer, Amy K; Stefansson, Hreinn...

   P Lo S Genetics, Vol. 8, Issue 5.

   Androgenetic alopecia (AGA) is a highly heritable condition and the most common form of hair loss in humans. Susceptibility loci have been described on the X chromosome and chromosome 20, but these... Read more

   Androgenetic alopecia (AGA) is a highly heritable condition and the most common form of hair loss in humans. Susceptibility loci have been described on the X chromosome and chromosome 20, but these loci explain a minority of its heritable variance. We conducted a large-scale meta-analysis of seven genome-wide association studies for early-onset AGA in 12,806 individuals of European ancestry. While replicating the two AGA loci on the X chromosome and chromosome 20, six novel susceptibility loci reached genome-wide significance (p = 2.62×10⁻⁹-1.01×10⁻¹²). Unexpectedly, we identified a risk allele at 17q21.31 that was recently associated with Parkinson's disease (PD) at a genome-wide significant level. We then tested the association between early-onset AGA and the risk of PD in a cross-sectional analysis of 568 PD cases and 7,664 controls. Early-onset AGA cases had significantly increased odds of subsequent PD (OR = 1.28, 95% confidence interval: 1.06-1.55, p = 8.9×10⁻³). Further, the AGA susceptibility alleles at the 17q21.31 locus are on the H1 haplotype, which is under negative selection in Europeans and has been linked to decreased fertility. Combining the risk alleles of six novel and two established susceptibility loci, we created a genotype risk score and tested its association with AGA in an additional sample. Individuals in the highest risk quartile of a genotype score had an approximately six-fold increased risk of early-onset AGA [odds ratio (OR) = 5.78, p = 1.4×10⁻⁸⁸]. Our results highlight unexpected associations between early-onset AGA, Parkinson's disease, and decreased fertility, providing important insights into the pathophysiology of these conditions. Read less

   Journal Article  |  Full Text Online

2. No genetic support for a contribution of prostaglandins to the aetiology of androgenetic alopecia 2013

   https://ncsu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3di9QwEB_kDsQXv9H6sUQR8aVeN2na9PFuz1MEF06UQ1_CZJOAH2yX6y745zuTtnu7oCC-9SEpbWYm-U3m4wfwAl3UISpPllZgThoS8sZ7lTu9IPvCyJGu_cucK6qvvj_E9sKNLSPt12zg6LrRyI_cd_96KmXDuy-BGCZtOPmyEz8odF98whdxpGNDT6G9mXsn0SEv6i_OjMSOFif2rBZ_gp07KFYOx9DZLQjjD6TsE-Y82E3DP0qtD1O_i7HN43_97G24OeBUcdwr1h24FpZ34fqHIRJ_D3DeCtI9LoEU3WbFKF4Q_hUoUvL7wKIl2ihWXFeCiSrk27IT61YQ5hQY1n2hDA9B7powvg1_tqtAGnMfPp-9-TR7lw90DflCEQrMfVkqU8rgGyOdq7zBqKRxsarrKgRtaqMxBl37yhSLhXGFI--7DJEgo6ZD0amHIAyWwZBvbFRZl41qTO0bb2Lli1CgwiKD56PM7Kpvx2FHN4ZWyaZVyuBlkuZ2BF7-4Py1WtuL-Vur5-fFefPxwp5mMNkT93aCrMnLm8ppBs9G-VsyO46l4DK0m85OuaFvpcjdyuBBrxhXsxX5vLKpMniVZPr3L7Un70_Tw6N_H_oYbshEycEpw0_gYH25CU_hgFVtAofHs9nX-SQZw29CIwuo

   Heilmann, S.; Nyholt, D.R.; Brockschmidt, F.F.; Hillmer, A.M.; Herold, C....

   British Journal Of Dermatology (1951), Vol. 169, Issue 1, pp. 222 - 224.

   Journal Article  |  Full Text Online

3. Paper of note in Science Translational Medicine 2016

   https://ncsu.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1LSwMxEB6kJy--KvhmDuJBCI3NPpJjFRdBBA-Cx2VqEhF0W0o9-O9NZrNlFQ_1HsLkMZnXN18Azmnqc-eVDZomSYQb4oSxVolp_hL0i3ysdP1M5qx4tn9V8FN7S4QyBE-U6HVcGqbXNjLy5F_fV92rGww1_0gWYvJcRJK7VMH8c4aeDWqZodiYVNvw3LXkMIYk_lzQB9OPmMCQWSt6ZI3riLwDW8m_xEl7IXZhwzV7MJw0Ibb--MILZMQnp9KHMHqkuVvgzGMzWzp8azBpOrIFe095QnxI9fd9uKpun27uRLeset5yVdTs44-LeiVSnURSB4CaMqdDJKpVVmZGGV1aY7UvrHSSFMlDuFx_wqP_DD6GzeB5FIy5Kk9gsFx8ulMYxJ0-43P9BsO_qvY

   Ferrarelli, Leslie K.

   Science Signaling, Vol. 9, Issue 431.

   Abstract only This week’s article describes how gene variant analysis might inform drug development. CARDIOVASCULAR GENOMICS At risk by association A missense variant in GLP1R associated with lower... Read more

   Abstract only This week’s article describes how gene variant analysis might inform drug development. CARDIOVASCULAR GENOMICS At risk by association A missense variant in GLP1R associated with lower fasting glucose levels and protective against type 2 diabetes is associated with lower risk of coronary heart disease, suggesting that GLP1R agonists are not associated with an unacceptable increase in cardiovascular risk. R. A. Scott, D. F. Freitag, L. Li, A. Y. Chu, P. Surendran, R. Young, N. Grarup, A. Stancáková, Y. Chen, T. V. Varga, H. Yaghootkar, J. Luan, J. H. Zhao, S. M. Willems, J. Wessel, S. Wang, N. Maruthur, K. Michailidou, A. Pirie, S. J. van der Lee, C. Gillson, A. A. Al Olama, P. Amouyel, L. Arriola, D. Arveiler, I. Aviles-Olmos, B. Balkau, A. Barricarte, I. Barroso, S. B. Garcia, J. C. Bis, S. Blankenberg, M. Boehnke, H. Boeing, E. Boerwinkle, I. B. Borecki, J. Bork-Jensen, S. Bowden, C. Caldas, M. Caslake, The CVD50 consortium, L. A. Cupples, C. Cruchaga, J. Czajkowski, M. den Hoed, J. A. Dunn, H. M. Earl, G. B. Ehret, E. Ferrannini, J. Ferrieres, T. Foltynie, I. Ford, N. G. Forouhi, F. Gianfagna, C. Gonzalez, S. Grioni, L. Hiller, J.-H. Jansson, M. E. Jørgensen, J. W. Jukema, R. Kaaks, F. Kee, N. D. Kerrison, T. J. Key, J. Kontto, Z. Kote-Jarai, A. T. Kraja, K. Kuulasmaa, J. Kuusisto, A. Linneberg, C. Liu, G. Marenne, K. L. Mohlke, A. P. Morris, K. Muir, M. Müller-Nurasyid, P. B. Munroe, C. Navarro, S. F. Nielsen, P. M. Nilsson, B. G. Nordestgaard, C. J. Packard, D. Palli, S. Panico, G. M. Peloso, M. Perola, A. Peters, C. J. Poole, J. R. Quirós, O. Rolandsson, C. Sacerdote, V. Salomaa, M.-J. Sánchez, N. Sattar, S. J. Sharp, R. Sims, N. Slimani, J. A. Smith, D. J. Thompson, S. Trompet, R. Tumino, D. L. van der A, Y. T. van der Schouw, J. Virtamo, M. Walker, K. Walter, GERAD_EC Consortium, Neurology Working Group of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE), Alzheimer’s Disease Genetics Consortium, Pancreatic Cancer Cohort Consortium, European Prospective Investigation into Cancer and Nutrition–Cardiovascular Disease (EPIC-CVD),EPIC-InterAct, J. E. Abraham, L. T. Amundadottir, J. L. Aponte, A. S. Butterworth, J. Dupuis, D. F. Easton, R. A. Eeles, J. Erdmann, P. W. Franks, T. M. Frayling, T. Hansen, J. M. M. Howson, T. Jørgensen, J. Kooner, M. Laakso, C. Langenberg, M. I. McCarthy, J. S. Pankow, O. Pedersen, E. Riboli, J. I. Rotter, D. Saleheen, N. J. Samani, H. Schunkert, P. Vollenweider, S. O’Rahilly, CHARGE consortium, The CHD Exome+ Consortium, CARDIOGRAM Exome Consortium, P. Deloukas, J. Danesh, M. O. Goodarzi, S. Kathiresan, J. B. Meigs, M. G. Ehm, N. J. Wareham, D. M. Waterworth, A genomic approach to therapeutic target validation identifies a glucose-lowering GLP1R variant protective for coronary heart disease. Sci. Transl. Med. 8 , 341ra76 (2016). [Abstract] Read less

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