Transcranial Direct Current Stimulation as an Add-on Treatment to Cognitive-Behavior Therapy in First Episode Drug-Naïve Major Depression Patients: The ESAP Study Protocol

Carvalho, Sandra; Gonçalves, Óscar F.; Brunoni, André R.; Fernandes-Gonçalves, Ana; Fregni, Felipe; Leite, Jorge

doi:10.3389/fpsyt.2020.563058

Cited by 10 publications

(4 citation statements)

References 81 publications

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“…However, about 15-30% of patients with depression do not respond to guideline-recommended therapies 14 . Novel augmentation treatments, such as non-invasive procedures like transcranial direct current stimulation (tDCS) [15][16][17][18] , have been developed in the last three decades to address non-response 19,20 .…”

Section: Effects Of Left Anodal Transcranial Direct Current Stimulati...mentioning

confidence: 99%

Effects of left anodal transcranial direct current stimulation on hypothalamic–pituitary–adrenal axis activity in depression: a randomized controlled pilot trial

Pedraz-Petrozzi

Sardinha

Gilles

et al. 2023

Sci Rep

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The main objective of this study was to evaluate the effect of left anodal transcranial direct current stimulation (tDCS) on hypothalamic–pituitary–adrenal axis (HPAA) activity in individuals with depression. We conducted a 3-week, randomized, triple-blind pilot trial with 47 participants (dropout rate: 14.89%) randomly assigned to either the tDCS or control group (sham stimulation). Salivary cortisol was used as an HPAA activity marker since cortisol is the effector hormone of the HPAA. The primary outcome was the effect of tDCS on the diurnal cortisol pattern (DCP and area under the curve with respect to ground -AUCg-). Secondary outcomes included tDCS effects on cortisol awakening response (CAR) and cortisol decline (CD), as well as the variation of cortisol concentrations between the initiation of tDCS and 2 weeks later. Intention-to-treat and per-protocol analyses were conducted. Our primary outcome showed an absent effect of tDCS on DCP and AUCg. Additionally, tDCS had an absent effect on CAR, CD, and cortisol concentration variation before-after stimulation. Our pilot study suggests that anodal tDCS showed an absent effect on HPAA activity in individuals with depression. More studies are needed to confirm these findings.

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Section: Effects Of Left Anodal Transcranial Direct Current Stimulati...mentioning

confidence: 99%

Effects of left anodal transcranial direct current stimulation on hypothalamic–pituitary–adrenal axis activity in depression: a randomized controlled pilot trial

Pedraz-Petrozzi

Sardinha

Gilles

et al. 2023

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Moreover, accumulating intervention studies have provided evidence of a causal relationship between FAA and MDD. For example, targeting to decrease the FAA, studies adapted neurofeedback training ( Peeters et al, 2014 ; Mirski et al, 2015 ; Wang et al, 2016 ), tDCS ( Mirski et al, 2015 ; Al-Kaysi et al, 2017 ; Carvalho et al, 2020 ), and repetitive TMS (rTMS) ( Olejarczyk et al, 2021 ) have found symptoms alleviations in MDD patients. Regarding the abnormal FAA in MDD patients, some recent studies explored whether it could predict the response to medication treatments but found mixed results ( Baskaran et al, 2018 ), and a meta-analysis suggested that individual differences (such as sex and age), clinical characteristics (such as medication and comorbidities), and specific measurements (such as electrode selection and normalization methods) affected FAA in MDD patients ( Van Der Vinne et al, 2017 ), indicating that it is essential to consider more factors when discussing abnormal FAA in MDD patients.…”

Section: The Neural Mechanisms Of Tacs For Treating Mddmentioning

confidence: 99%

Transcranial alternating current stimulation for the treatment of major depressive disorder: from basic mechanisms toward clinical applications

Pan,

Ye,

Zhong

et al. 2023

Front. Hum. Neurosci.

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Non-pharmacological treatment is essential for patients with major depressive disorder (MDD) that is medication resistant or who are unable to take medications. Transcranial alternating current stimulation (tACS) is a non-invasive brain stimulation method that manipulates neural oscillations. In recent years, tACS has attracted substantial attention for its potential as an MDD treatment. This review summarizes the latest advances in tACS treatment for MDD and outlines future directions for promoting its clinical application. We first introduce the neurophysiological mechanism of tACS and its novel developments. In particular, two well-validated tACS techniques have high application potential: high-definition tACS targeting local brain oscillations and bifocal tACS modulating interarea functional connectivity. Accordingly, we summarize the underlying mechanisms of tACS modulation for MDD. We sort out the local oscillation abnormalities within the reward network and the interarea oscillatory synchronizations among multiple MDD-related networks in MDD patients, which provide potential modulation targets of tACS interventions. Furthermore, we review the latest clinical studies on tACS treatment for MDD, which were based on different modulation mechanisms and reported alleviations in MDD symptoms. Finally, we discuss the main challenges of current tACS treatments for MDD and outline future directions to improve intervention target selection, tACS implementation, and clinical validations.

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“…Major depressive disorder (MDD) is a common psychiatric condition, and it is predicted that MDD affects ~264 million individuals globally ( 1 , 2 ). In China, the incidence of MDD is ~3.4%, and in the USA, the incidence is up to 16.2%, causing a heavy burden for the families of patients with MDD and the nation as a whole ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

CB1 receptor mediates anesthetic drug ketamine‑induced neuroprotection against glutamate in HT22 cells

Bao,

Wang,

Xue

et al. 2024

Exp Ther Med

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The anesthetic drug, ketamine (KTM) has been shown to induce therapeutic effects against major depressive disorder (MDD), however the related underlying mechanisms remain unclear. In the present study, HT22 neuronal cells were treated with glutamate to imitate oxidative stress injury in MDD, and it was hypothesized that the cannabinoid type 1 (CB1) receptor mediates KTM-induced neuroprotection via ameliorating mitochondrial function in glutamate-treated neuronal cells. Compared with the control, glutamate decreased cell viability and intracellular antioxidants, including glutathione (GSH), catalase and superoxide dismutase 2 levels, and inhibited mitochondrial function simultaneously. Moreover, glutamate increased lactate dehydrogenase release, cellular apoptosis level, cleaved caspase-3 expression and intracellular oxidants, such as reactive oxygen species, oxidized GSH and mitochondrial superoxide in the cells. The presence of KTM, however, significantly decreased the glutamate-induced oxidative stress injury, ameliorated the antioxidant/oxidant levels in the cells, enhanced mitochondrial function and upregulated CB1 receptor expression (P<0.05). Co-administration of the CB1 receptor antagonist AM251 markedly abolished the KTM-induced cytoprotective effects and ameliorations of antioxidant/oxidant levels and mitochondrial function, and also reversed CB1 upregulation (P<0.05). These observations indicated that KTM decreases the oxidative stress injury caused by glutamate in HT22 neuronal cells, and the neuroprotective effects may be mediated by the CB1 receptor.

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Transcranial Direct Current Stimulation as an Add-on Treatment to Cognitive-Behavior Therapy in First Episode Drug-Naïve Major Depression Patients: The ESAP Study Protocol

Cited by 10 publications

References 81 publications

Effects of left anodal transcranial direct current stimulation on hypothalamic–pituitary–adrenal axis activity in depression: a randomized controlled pilot trial

Effects of left anodal transcranial direct current stimulation on hypothalamic–pituitary–adrenal axis activity in depression: a randomized controlled pilot trial

Transcranial alternating current stimulation for the treatment of major depressive disorder: from basic mechanisms toward clinical applications

CB1 receptor mediates anesthetic drug ketamine‑induced neuroprotection against glutamate in HT22 cells

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