Major Depressive Disorder Classification Based on Different Convolutional Neural Network Models: Deep Learning Approach

2020 ◽  
Vol 52 (1) ◽  
pp. 38-51
Author(s):  
Caglar Uyulan ◽  
Türker Tekin Ergüzel ◽  
Huseyin Unubol ◽  
Merve Cebi ◽  
Gokben Hizli Sayar ◽  
...  

The human brain is characterized by complex structural, functional connections that integrate unique cognitive characteristics. There is a fundamental hurdle for the evaluation of both structural and functional connections of the brain and the effects in the diagnosis and treatment of neurodegenerative diseases. Currently, there is no clinically specific diagnostic biomarker capable of confirming the diagnosis of major depressive disorder (MDD). Therefore, exploring translational biomarkers of mood disorders based on deep learning (DL) has valuable potential with its recently underlined promising outcomes. In this article, an electroencephalography (EEG)-based diagnosis model for MDD is built through advanced computational neuroscience methodology coupled with a deep convolutional neural network (CNN) approach. EEG recordings are analyzed by modeling 3 different deep CNN structure, namely, ResNet-50, MobileNet, Inception-v3, in order to dichotomize MDD patients and healthy controls. EEG data are collected for 4 main frequency bands (Δ, θ, α, and β, accompanying spatial resolution with location information by collecting data from 19 electrodes. Following the pre-processing step, different DL architectures were employed to underline discrimination performance by comparing classification accuracies. The classification performance of models based on location data, MobileNet architecture generated 89.33% and 92.66% classification accuracy. As to the frequency bands, delta frequency band outperformed compared to other bands with 90.22% predictive accuracy and area under curve (AUC) value of 0.9 for ResNet-50 architecture. The main contribution of the study is the delineation of distinctive spatial and temporal features using various DL architectures to dichotomize 46 MDD subjects from 46 healthy subjects. Exploring translational biomarkers of mood disorders based on DL perspective is the main focus of this study and, though it is challenging, with its promising potential to improve our understanding of the psychiatric disorders, computational methods are highly worthy for the diagnosis process and valuable in terms of both speed and accuracy compared with classical approaches.

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Naho Ichikawa ◽  
Giuseppe Lisi ◽  
Noriaki Yahata ◽  
Go Okada ◽  
Masahiro Takamura ◽  
...  

Abstract The limited efficacy of available antidepressant therapies may be due to how they affect the underlying brain network. The purpose of this study was to develop a melancholic MDD biomarker to identify critically important functional connections (FCs), and explore their association to treatments. Resting state fMRI data of 130 individuals (65 melancholic major depressive disorder (MDD) patients, 65 healthy controls) were included to build a melancholic MDD classifier, and 10 FCs were selected by our sparse machine learning algorithm. This biomarker generalized to a drug-free independent cohort of melancholic MDD, and did not generalize to other MDD subtypes or other psychiatric disorders. Moreover, we found that antidepressants had a heterogeneous effect on the identified FCs of 25 melancholic MDDs. In particular, it did impact the FC between left dorsolateral prefrontal cortex (DLPFC)/inferior frontal gyrus (IFG) and posterior cingulate cortex (PCC)/precuneus, ranked as the second ‘most important’ FC based on the biomarker weights, whilst other eight FCs were normalized. Given that left DLPFC has been proposed as an explicit target of depression treatments, this suggest that the limited efficacy of antidepressants might be compensated by combining therapies with targeted treatment as an optimized approach in the future.


2015 ◽  
Vol 78 (1) ◽  
pp. 58-66 ◽  
Author(s):  
Martina Papmeyer ◽  
Stephen Giles ◽  
Jessica E. Sussmann ◽  
Shauna Kielty ◽  
Tiffany Stewart ◽  
...  

2003 ◽  
Vol 33 (7) ◽  
pp. 1319-1323 ◽  
Author(s):  
B. MANGWETH ◽  
J. I. HUDSON ◽  
H. G. POPE ◽  
A. HAUSMANN ◽  
C. De COL ◽  
...  

Background. Family studies have suggested that eating disorders and mood disorders may coaggregate in families. To study further this question, data from a family interview study of probands with and without major depressive disorder was examined.Method. A bivariate proband predictive logistic regression model was applied to data from a family interview study, conducted in Innsbruck, Austria, of probands with (N=64) and without (N=58) major depressive disorder, together with 330 of their first-degree relatives.Results. The estimated odds ratio (OR) for the familial aggregation of eating disorders (anorexia nervosa, bulimia nervosa and binge-eating disorder) was 7·0 (95% CI 1·4, 28; P=0·006); the OR for the familial aggregation of mood disorders (major depression and bipolar disorder) was 2·2 (0·92, 5·4; P=0·076); and for the familial coaggregation of eating disorders with mood disorders the OR was 2·2 (1·1, 4·6; P=0·035).Conclusions. The familial coaggregation of eating disorders with mood disorders was significant and of the same magnitude as the aggregation of mood disorders alone – suggesting that eating disorders and mood disorders have common familial causal factors.


CNS Spectrums ◽  
2013 ◽  
Vol 18 (5) ◽  
pp. 231-241 ◽  
Author(s):  
Mark J. Niciu ◽  
Dawn F. Ionescu ◽  
Daniel C. Mathews ◽  
Erica M. Richards ◽  
Carlos A. Zarate

The etiopathogenesis and treatment of major mood disorders have historically focused on modulation of monoaminergic (serotonin, norepinephrine, dopamine) and amino acid [γ-aminobutyric acid (GABA), glutamate] receptors at the plasma membrane. Although the activation and inhibition of these receptors acutely alter local neurotransmitter levels, their neuropsychiatric effects are not immediately observed. This time lag implicates intracellular neuroplasticity as primary in the mechanism of action of antidepressants and mood stabilizers. The modulation of intracellular second messenger/signal transduction cascades affects neurotrophic pathways that are both necessary and sufficient for monoaminergic and amino acid–based treatments. In this review, we will discuss the evidence in support of intracellular mediators in the pathophysiology and treatment of preclinical models of despair and major depressive disorder (MDD). More specifically, we will focus on the following pathways: cAMP/PKA/CREB, neurotrophin-mediated (MAPK and others), p11, Wnt/Fz/Dvl/GSK3β, and NFκB/ΔFosB. We will also discuss recent discoveries with rapidly acting antidepressants, which activate the mammalian target of rapamycin (mTOR) and release of inhibition on local translation via elongation factor stimulation. Throughout this discourse, we will highlight potential intracellular targets for therapeutic intervention. Finally, future clinical implications are discussed.


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