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Comorbidity between Alzheimer’s disease and Major Depression: a behavioural and transcriptomic characterization study in mice

ABSTRACT: Comorbidity between Alzheimer’s disease and Major Depression: a behavioural and transcriptomic characterization study in mice

PROVIDER: PRJNA705183 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13794800_1.fastq.gz	Fastqsanger.gz
	SRR13794800_2.fastq.gz	Fastqsanger.gz
	SRR13794900_1.fastq.gz	Fastqsanger.gz
	SRR13794900_2.fastq.gz	Fastqsanger.gz
	SRR13795000_1.fastq.gz	Fastqsanger.gz

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Comorbidity between Alzheimer’s disease and Major Depression: a behavioural and transcriptomic characterization study in mice

Project description:Background: Major Depression (MD) is the most prevalent psychiatric disease in the population and is considered a prodromal stage of the Alzheimer’s disease (AD). Despite both diseases having a robust genetic component, the common transcriptomic signature remains unknown. Method: In this regard, we investigated the cognitive and emotional behavioural responses in 3- (n=16 per group) and 6-month-old (n=14 per group) in APP/PSEN1-Tg mutant mice, before -amyloid plaques were detected in comparison with non-transgenic mice. Then, we studied the deregulation of genes and pathways in prefrontal cortex, striatum, hippocampus and amygdala of mice at both ages, using transcriptomic and functional data analysis. Results: We found that depressive-like and anxiety-like behaviours, as well as memory impairments are already present at 3-month-old APP/PSEN1-Tg mutant mice together with the deregulation of several genes such as Ciart, Chrm5, Aldh1a, Grin3b, Nr1d1 and Mc4r, and gene sets, including components of the circadian rhythms, electronic transport chain, neuroinflammation and neurotransmission. Then, we extended these results to human data performing GSEA analysis using DisGeNET database, which is specific for diseases and disease-related phenotypes and provides translational support for common deregulated gene sets related to MD and AD. Conclusion: The present study shed further light on the genetic bases shared between MD and AD, illustrating a wide characterization from the behavioural to transcriptomic level in APP/PSEN1-Tg mutant mouse model. These findings could indicate that late MD could be an early manifestation of AD.

2022-01-17 | GSE167739 | GEO

The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

Project description:While depression and chronic pain are frequently comorbid, underlying neuronal circuits, and their relevance for the understanding of psychopathology, remain poorly defined. Here we show in mice that hyperactivity of the neuronal pathway linking the basolateral amygdala to the anterior cingulate cortex is essential for chronic pain-induced depression. In naive male mice, we demonstrate that activation of this pathway is sufficient to trigger depressive-like behaviors, as well as transcriptomic alterations that recapitulate core molecular features of depression in the human brain. These alterations notably impact gene modules related to myelination and the oligodendrocyte lineage. Among these, we show that Sema4a, a hub gene significantly upregulated in both male mice and humans in the context of altered mood, is necessary for the emergence of depressive-like behaviors. Overall, these results place the BLA-ACC pathway at the core of pain and depression comorbidity, and unravel the role of impaired myelination and Sema4a in mood control.

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Major depression MDD suicide brain study

Project description:Background: Major Depressive Disorder (MDD) represents a major social and economic health issue and constitutes a major risk factor for MDD suicide. The molecular pathology of suicidal depression remains poorly understood, although it has been hypothesized that regulatory genomic processes are involved in the pathology of both MDD and suicidality. Methods: Genome-wide patterns of DNA methylation were assessed in depressed MDD suicide completers (n=20) and compared to non-psychiatric, sudden-death controls (n=20) using tissue from two cortical brain regions (Brodmann Area 11 (BA11) and Brodmann Area 25 (BA25)). Analyses focussed on identifying differentially methylated regions (DMRs) associated with suicidal depression, and epigenetic variation was explored in the context of polygenic risk scores for major depression and MDD suicide. Weighted gene co-methylation network analysis was used to identify modules of co-methylated loci associated with depressed MDD suicide completers and polygenic burden for MDD and MDD suicide attempt. Results: We identified a DMR upstream of the PSORS1C3 gene, subsequently validated using bisulfite-pyrosequencing and replicated in a second set of MDD suicide samples, which is characterized by significant hypomethylation in both cortical brain regions in MDD MDD suicide cases. We also identified discrete modules of co-methylated loci associated with polygenic risk burden for MDD suicide attempt, but not major depression. MDD suicide-associated co-methylation modules were enriched among gene networks implicating biological processes relevant to depression and suicidality, including nervous system development and mitochondria function. Conclusions: Our data suggest there are coordinated changes in DNA methylation associated with MDD suicide that may offer novel insights into the molecular pathology associated with depressed MDD suicide completers.

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Whole Genome Sequencing in Psychotic Major Depression

Project description:Whole Genome Sequencing in Psychotic Major Depression

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Peripheral whole blood: Healthy control and Major depression disorder patients

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Expression data from peripheral blood lymphocytes of major depression, subsyndromal symptomatic depression, and healthy controls

Project description:Several studies have suggested that SSD is a transitory phenomena in the depression spectrum and is thus considered a subtype of depression. However, the pathophysioloy of depression remain largely obscure and studies on SSD are limited. The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among drug-free first-episode subjects with SSD, MDD, and healthy controls. We used microarrays to detail the global programme of gene expression to develop blood-based gene expression profiles models for classification of subsyndromal symptomatic depression and major depressive disorder The present study compared the expression profile and made the classification with the leukocytes by using whole-genome cRNA microarrays among drug-free first-episode subjects with SSD, MDD, and matched controls (8 subjects in each group). Support vector machines (SVMs) were utilized for training and testing on candidate signature expression profiles from signature selection step.

2012-03-21 | E-GEOD-32280 | biostudies-arrayexpress

MicroRNAs as diagnostic biomarkers for major depression

Project description:Blood samples taken from healthy controls and patients with major depression were analyzed for differences in microRNA expression. Patients were treated with either electroconvulsive therapy or ketamine and samples were again analyzed to determine if these treatments affected microRNA expression. Baseline microRNA expression profiles were studied to see if they could predict treatment response.

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Integration of Genomics & Transcriptomics in Normal Twins & Major Depression

Project description:Integration of Genomics & Transcriptomics in Normal Twins & Major Depression

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