Psychological status in depressive patients correlates with metabolic gene expression

Alcocer-Gómez, Elísabet; Barquero, N. Casas; Núñez-Vasco, Jéssica; Navarro‐Pando, José M.; Bullón, Pedro

doi:10.1111/cns.12755

Cited by 24 publications

(14 citation statements)

References 10 publications

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“…Autophagy has been frequently discussed in the researches of depression about human and animal. A small sample-size study found higher expression of autophagy genes in blood mononuclear cells from depression patients than that from healthy controls [ 10 ], and another study presented the positive correlation between the expression of Beclin1 in these cells and clinical treatment success [ 11 ]. Since the hippocampus is one of the key brain areas where depression develops, autophagy is often discovered in this location.…”

Section: Introductionmentioning

confidence: 99%

EA Ameliorated Depressive Behaviors in CUMS Rats and Was Related to Its Suppressing Autophagy in the Hippocampus

et al. 2020

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Autophagy is confirmed to be involved in the onset and development of depression, and some antidepressants took effect by influencing the autophagic process. Electroacupuncture (EA), as a common complementary treatment for depression, may share the mechanism of influencing autophagy in the hippocampus like antidepressants. To investigate that, sixty Sprague-Dawley rats firstly went through chronic unpredictable mild stress (CUMS) model establishment, and 15 rats were assigned to a control group. After modeling, 45 successfully CUMS-induced rats were randomly divided to 3 groups: CUMS, selective serotonin reuptake inhibitor (SSRI), and EA groups (15 rats per group), to accept different interventions for 2 weeks. A sucrose preference test (SPT), weighing, and open field test (OFT) were measurement for depressive behaviors of rats. Transmission electron microscope (TEM), immunohistochemistry (IHC), and western blot analysis were used to evaluate the autophagic changes. After that, depression-like behaviors were successfully induced in CUMS models and reversed by SSRI and EA treatments (both p<0.05), but these two therapies had nonsignificant difference between each other (p>0.05). Autolysosomes observed through TEM in the CUMS group were more than that in the control group. Their number and size in the SSRI and EA groups also decreased significantly. From IHC, the CUMS group showed enhanced positive expression of both Beclin1 and LC3 in CA1 after modeling (p<0.05), and the LC3 level declined after EA treatments, which was verified by decreased LC3-II/LC3-I in western blot analysis. We speculated that CUMS-induced depression-like behavior was interacted with an autophagy process in the hippocampus, and EA demonstrated antidepressant effects by partly inhibiting autophagy with a decreased number of autolysosomes and level of LC3 along with LC3-II/LC3-I.

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Section: Introductionmentioning

confidence: 99%

EA Ameliorated Depressive Behaviors in CUMS Rats and Was Related to Its Suppressing Autophagy in the Hippocampus

et al. 2020

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“…Intriguingly, a profound body of evidence illustrates autophagy to be crucially involved in depression [ 69 ]. Alcocer-Gómez et al, for instance, reported the expression of autophagy proteins to be upregulated in MDD patients [ 70 ]. Moreover, expression of autophagy proteins (i.e., Beclin-1 and light chain 3-II/I (LC3-II/I)) was shown to be elevated in the rat hippocampus following ECS treatment [ 71 ], leading Gassen and Rein to hypothesize that autophagic mechanisms (although already heightened at baseline) might still be insufficient in some disease cases [ 69 ].…”

Section: Discussionmentioning

confidence: 99%

Novel candidate genes for ECT response prediction—a pilot study analyzing the DNA methylome of depressed patients receiving electroconvulsive therapy

et al. 2020

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Background Major depressive disorder (MDD) represents a serious global health concern. The urge for efficient MDD treatment strategies is presently hindered by the incomplete knowledge of its underlying pathomechanism. Despite recent progress (highlighting both genetics and the environment, and thus DNA methylation, to be relevant for its development), 30–50% of MDD patients still fail to reach remission with standard treatment approaches. Electroconvulsive therapy (ECT) is one of the most powerful options for the treatment of pharmacoresistant depression; nevertheless, ECT remission rates barely reach 50% in large-scale naturalistic population-based studies. To optimize MDD treatment strategies and enable personalized medicine in the long- term, prospective indicators of ECT response are thus in great need. Because recent target-driven analyses revealed DNA methylation baseline differences between ECT responder groups, we analyzed the DNA methylome of depressed ECT patients using next-generation sequencing. In this pilot study, we did not only aim to find novel targets for ECT response prediction but also to get a deeper insight into its possible mechanism of action. Results Longitudinal DNA methylation analysis of peripheral blood mononuclear cells isolated from a cohort of treatment-resistant MDD patients ( n = 12; time points: before and after 1st and last ECT, respectively) using a TruSeq-Methyl Capture EPIC Kit for library preparation, led to the following results: (1) The global DNA methylation differed neither between the four measured time points nor between ECT responders ( n = 8) and non-responders ( n = 4). (2) Analyzing the DNA methylation variance for every probe (=1476812 single CpG sites) revealed eight novel candidate genes to be implicated in ECT response (protein-coding genes: RNF175 , RNF213 , TBC1D14 , TMC5 , WSCD1 ; genes encoding for putative long non-coding RNA transcripts: AC018685.2 , AC098617.1 , CLCN3P1 ). (3) In addition, DNA methylation of two CpG sites (located within AQP10 and TRERF1 ) was found to change during the treatment course. Conclusions We suggest ten novel candidate genes to be implicated in either ECT response or its possible mechanism. Because of the small sample size of our pilot study, our findings must be regarded as preliminary.

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“…Interest in the role of autophagy in the context of stress-related and psychiatric conditions, particularly neuronal autophagy, has grown considerably. Altered autophagy gene expression has been reported in individuals with major depressive disorder (MDD; Alcocer-Gomez et al, 2017 ). Furthermore, antidepressants induce autophagy in the brain and reverse biochemical and behavioral signs of stress-induced MDD ( Gulbins et al, 2018 ).…”

Section: Autophagy and Neurological/psychiatric Diseasementioning

confidence: 99%

Gut Microbiome Regulation of Autophagic Flux and Neurodegenerative Disease Risks

et al. 2021

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The gut microbiome-brain axis exerts considerable influence on the development and regulation of the central nervous system. Numerous pathways have been identified by which the gut microbiome communicates with the brain, falling largely into the two broad categories of neuronal innervation and immune-mediated mechanisms. We describe an additional route by which intestinal microbiology could mediate modifiable risk for neuropathology and neurodegeneration in particular. Autophagy, a ubiquitous cellular process involved in the prevention of cell damage and maintenance of effective cellular function, acts to clear and recycle cellular debris. In doing so, autophagy prevents the accumulation of toxic proteins and the development of neuroinflammation, both common features of dementia. Levels of autophagy are influenced by a range of extrinsic exposures, including nutrient deprivation, infection, and hypoxia. These relationships between exposures and rates of autophagy are likely to be mediated, as least in part, by the gut microbiome. For example, the suppression of histone acetylation by microbiome-derived short-chain fatty acids appears to be a major contributor to upregulation of autophagic function. We discuss the potential contribution of the microbiome-autophagy axis to neurological health and examine the potential of exploiting this link to predict and prevent neurodegenerative diseases.

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Psychological status in depressive patients correlates with metabolic gene expression

Cited by 24 publications

References 10 publications

EA Ameliorated Depressive Behaviors in CUMS Rats and Was Related to Its Suppressing Autophagy in the Hippocampus

EA Ameliorated Depressive Behaviors in CUMS Rats and Was Related to Its Suppressing Autophagy in the Hippocampus

Novel candidate genes for ECT response prediction—a pilot study analyzing the DNA methylome of depressed patients receiving electroconvulsive therapy

Gut Microbiome Regulation of Autophagic Flux and Neurodegenerative Disease Risks

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