مقاله انگلیسی رایگان در مورد فارماکوژنومیک در درمان اختلالات خلقی – اسپرینگر 2017

 

مشخصات مقاله
انتشار مقاله سال 2017
تعداد صفحات مقاله انگلیسی 17 صفحه
هزینه دانلود مقاله انگلیسی رایگان میباشد.
منتشر شده در نشریه اسپرینگر
نوع مقاله ISI
عنوان انگلیسی مقاله Pharmacogenomics in the treatment of mood disorders: Strategies and Opportunities for personalized psychiatry
ترجمه عنوان مقاله فارماکوژنومیک در درمان اختلالات خلقی: استراتژی ها و فرصت هایی برای روانپزشکی شخصی
فرمت مقاله انگلیسی  PDF
رشته های مرتبط روانشناسی، پزشکی
گرایش های مرتبط روانشناسی بالینی، روانپزشکی
مجله EPMA Journa
دانشگاه Discipline of Psychiatry – University of Adelaide – Australia
کلمات کلیدی روانپزشکی شخصی، لیتیم، SSRIs، فارماکوژنومیک، افسردگی ،اختلال دو قطبی، داروهای پیشگیرانه
کلمات کلیدی انگلیسی Personalized psychiatry, Lithium, SSRIs, Pharmacogenomics, Depression, Bipolar disorder, Predictive preventive and personalized medicine (PPPM)
شناسه دیجیتال – doi https://doi.org/10.1007/s13167-017-0112-8
کد محصول E8074
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Introduction

Mood disorders in psychiatry encompass a bipolar disorder (BPD), which is characterized by recurrent alternating episodes of elevated mood (mania) and depression, and a major depressive disorder (MDD), which is defined by symptoms associated with pervasively low mood. The clinical diagnosis of MDD is based on the presence of either depressed mood or loss of interest and pleasure (anhedonia) for at least 2 weeks, and requires additional symptoms such as weight loss, changes in appetite, insomnia or hypersomnia, psychomotor agitation or retardation, loss of energy or fatigue, feelings of worthlessness, poor concentration, and suicidal thoughts [5]. Both MDD and BPD are among the most disabling mental health disorders worldwide [34, 41, 85, 120] with a lifetime prevalence of ~ 12 [4] and 1% [80], respectively. Based on the 2013 global burden of diseases study by the Institute for Health Metrics and Evaluation at the University of Washington, MDD alone caused an estimated 61.6 million years of life lived with disability worldwide, accounting for 8.1% of the total years lived with disability (YLDs) and for 2.5% of the total disability-adjusted life years [33, 41, 85]. BPD contributed an additional 9.9 million years of life lived with disability [34]. The causes of mood disorders are complex and involve the interplay between genetic predisposition and non-genetic biological, psychological, and social factors. Both MDD and BPD are highly heritable, and genetic factors contribute 31– 42% of the disease risk in MDD [109] and 59–85% in BPD [71, 77]. Moreover, patients with MDD and BPD often show overlapping clinical features [25]. It is estimated that about 47% of the genetic risk factors are shared between MDD and BPD [21] and a shared genetic risk was revealed between mood disorders and other psychiatric and medical morbidities [3, 21, 22]. Environmental risk factors such as childhood abuse (physical, sexual, or psychological) are also frequently reported to be associated with both disorders [1]. Candidate gene and genome-wide association studies (GWASs) have identified a list of candidate genes for MDD [20, 24, 35, 59] and BPD [55, 84, 92, 106]. To date, GWAS approaches have identified 18 loci contributing to the risk of MDD [20, 24, 59] and over 8 loci associated with BPD [55, 63, 84, 92, 106], including shared genetic loci located in the CACNA1C, CACNB2, AS3MT, ITIH3, and CCDC68 genes [22]. An extension of the GWAS approaches such as polygenic score analysis [87], bivariate restricted maximum likelihood (REML) in genome-wide complex trait analysis (GCTA) [21] and linkage disequilibrium (LD) score regression have strongly suggested that mood disorders are polygenic in nature, in that multiple genetic variants interacting with environmental factors contribute to the development of the diseases [87].