دانلود مقاله ISI انگلیسی شماره 34491
عنوان فارسی مقاله

الکتروشوک درمانی (ECT)عامل نوروتروفیک مغزی سرم مشتق شده (BDNF) در بیماران مبتلا به افسردگی مقاوم به دارو را افزایش می دهد

کد مقاله سال انتشار مقاله انگلیسی ترجمه فارسی تعداد کلمات
34491 2015 5 صفحه PDF سفارش دهید محاسبه نشده
خرید مقاله
پس از پرداخت، فوراً می توانید مقاله را دانلود فرمایید.
عنوان انگلیسی
Electroconvulsive Therapy (ECT) increases serum Brain Derived Neurotrophic Factor (BDNF) in drug resistant depressed patients
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : European Neuropsychopharmacology, Volume 16, Issue 8, December 2006, Pages 620–624

کلمات کلیدی
الکتروشوک درمانی - افسردگی اساسی - سرم - مقاوم در برابر دارو -
پیش نمایش مقاله
پیش نمایش مقاله الکتروشوک درمانی (ECT)عامل نوروتروفیک مغزی سرم مشتق شده (BDNF) در بیماران مبتلا به افسردگی مقاوم به دارو  را افزایش می دهد

چکیده انگلیسی

Several findings have suggested that the neurotrophin BDNF could contribute to clinical efficacy of antidepressant treatments. The purpose of this study was to analyse if ECT operates a modulation of serum BDNF levels in a sample of drug resistant depressed patients. The results obtained show significantly higher serum levels of BDNF following ECT. More specifically, while no change occurred in the whole sample between T0 (baseline) and T1 (after ECT) (p = 0.543) a significant increase has been identified at T2, one month after the end of ECT (p = 0.002). However, the BDNF augmentation was evident even between T0 and T1 in a subgroup of patients who has low baseline BDNF levels. Although future researches are needed, the results herein presented show for the first time that ECT is associated with changes in serum BDNF and further support the possible involvement of BDNF in antidepressant therapies

مقدمه انگلیسی

Major depression is a severe and life-threatening illness which represents one of the most important causes of disability world-wide. In particular, about 50% of the affected patients experience a chronic course and up to 20% of them shows an insufficient response to drug treatments (Fava et al., 2003 and Hussain and Cochrane, 2004). As other chronic diseases, major depression is a complex disorder caused by the interaction between environmental and biological/genetic risk factors. Although the molecular alterations underlying the pathogenesis remains to be clearly established, recent preclinical and clinical studies have suggested an involvement of the neurotrophin Brain Derived Neurotrophic Factor (BDNF) in the aetiology of major depression as well as in the antidepressant drug treatment (Angelucci et al., 2005, Castren, 2004, Duman, 2004 and Hashimoto et al., 2004). BDNF is a neurotrophic factor widely expressed in the Central Nervous System (CNS) that plays a major role in brain development, survival and maintenance of neuronal functions and synaptic plasticity. Studies of brain imaging suggest that depressed patients have neuronal atrophy and cell loss in discrete brain regions (Bremner et al., 2000, Krishnan et al., 1993, Kumar et al., 1998, Kumar et al., 2000, Kumar et al., 2004 and Sheline et al., 1996), which are suggestive of a reduction in neuron plasticity. In line with these observations, different studies reported a reduction of BDNF expression in post-mortem brain of depressed subjects (Dwivedi et al., 2001, Dwivedi et al., 2003 and Molnar et al., 2003). Extensive research in rodents has shown that stress-related behaviours can alter the expression of BDNF in the limbic system and cortex (Roceri et al., 2002, Roceri et al., 2004, Smith and Cizza, 1996 and Vollmayr et al., 2001). Furthermore, antidepressant drug treatment enhances BDNF expression and production (Altar, 1999, Castren, 2004, Duman et al., 1997 and Nibuya et al., 1995) and the neurotrophin signalling appears to be required for antidepressant activity in animal models of depression (Castren, 2004, Saarelainen et al., 2003 and Sairanen et al., 2005). The involvement of BNDF in major depression and antidepressant treatment has gained further support from a series of biochemical studies in humans. A decrease in BDNF serum levels has been associated with major depression (Karege et al., 2002a), an effect that is normalized by antidepressant drug therapies (Aydemir et al., 2005 and Shimizu et al., 2003). Moreover a significant correlation between BDNF serum levels and depressive personality traits in a healthy subject was also found (Lang et al., 2004). Electroconvulsive Therapy (ECT) is one of the eligible therapies for the treatment of major depression (American Psychiatry Association, 2000 and UK ECT Review Group, 2003). Preclinical studies have shown that electroconvulsive seizures (ECS) produces a robust increase in BDNF mRNA (Altar et al., 2004, Chen et al., 2001, Duman et al., 1997, Nibuya et al., 1995 and Zetterstrom et al., 1997) and BDNF protein (Altar et al., 2003) in different rat brain areas. However, whether or not ECT could affect the peripheral levels of BDNF in depressed patients is still an open question. In order to address this issue, we investigated, in the present study, serum levels of BDNF in a group of drug resistant depressed patients before and after ECT.

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