{"id":8010,"date":"2011-04-23T22:05:06","date_gmt":"2011-04-24T02:05:06","guid":{"rendered":"http:\/\/1boringoldman.com\/?p=8010"},"modified":"2011-04-23T22:05:06","modified_gmt":"2011-04-24T02:05:06","slug":"personalized-medicine-a-conclusion-in-search-of-an-argument","status":"publish","type":"post","link":"https:\/\/1boringoldman.com\/index.php\/2011\/04\/23\/personalized-medicine-a-conclusion-in-search-of-an-argument\/","title":{"rendered":"personalized medicine: a conclusion in search of an argument…"},"content":{"rendered":"\n
Any scientist with access to the news is excited by the possibilities implicit in the amazing advances in genetics research in the recent decade, even up here in Georgia’s Appalachia. And each scientist puts their own twist on what might be up ahead. In Psychiatry, genetic markers have long been suspected to play a role in Schizophrenia , Manic Depressive Illness, Attention Deficit Disorder, etc. The possibility of finding those connections preoccupies many. But there are a lot of neuroscientists who think that there are genetic explanations that explain the variable response to medications seen with most psychopharmacologic agents. So the race is on to find those connections. I’ve previously looked at this study, but I know more now, so I want to revisit it. The full text of this article is available online here<\/font><\/strong><\/a>: <\/div>\n
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Prediction of Antidepressant Response to Milnacipran by Norepinephrine Transporter Gene Polymorphisms<\/font><\/strong>
by Keizo Yoshida, Hitoshi Takahashi, Hisashi Higuchi, Mitsuhiro Kamata, Ken-ichi Ito, Kazuhiro Sato, Shingo Naito, Tetsuo Shimizu, Kunihiko Itoh, Kazuyuki Inoue, Toshio Suzuki, Charles B. Nemeroff<\/sup>
American Journal of Psychiatry<\/font><\/strong> 2004; 161:1575–1580<\/div>\n

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Abstract<\/font><\/strong><\/em>:<\/div>\n
Objective<\/font><\/strong>: With a multitude of antidepressants available, predictors of response to different classes of antidepressants are of considerable interest. The purpose of the present study was to determine whether norepinephrine transporter gene (NET) and serotonin transporter gene (5-HTT) polymorphisms are associated with the antidepressant response to milnacipran, a dual serotonin\/norepinephrine reuptake inhibitor.<\/sup><\/div>\n
Method<\/font><\/strong>: Ninety-six Japanese patients with major depressive disorder were treated with milnacipran, 50–100 mg\/day, for 6 weeks. Severity of depression was assessed with the Montgomery-Åsberg Depression Rating Scale. Assessments were carried out at baseline and at 1, 2, 4, and 6 weeks of treatment. The method of polymerase chain reaction was used to determine allelic variants.<\/sup><\/div>\n
Results<\/font><\/strong>: Eighty patients completed the study. The presence of the T allele of the NET T-182C polymorphism was associated with a superior antidepressant response, whereas the A\/A genotype of the NET G1287A polymorphism was associated with a slower onset of therapeutic response. In contrast, no influence of 5-HTT polymorphisms on the antidepressant response to milnacipran was detected.<\/sup><\/div>\n
Conclusions<\/font><\/strong>: The results suggest that NET but not 5-HTT polymorphisms in part determine the antidepressant response to milnacipran.<\/sup><\/div>\n<\/blockquote>\n
96 Japanese patients with Major Depressive Disorder<\/font><\/strong> were treated with an SRNI<\/font><\/strong> [malnicipran]. Since we are sure to be bombarded with biomarkers studies, I thought I’d run through a few quick steps for vetting them as they come along.<\/div>\n

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Who paid for the study?<\/font><\/strong><\/u><\/div>\n