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Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

ABSTRACT: Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

PROVIDER: PRJNA1159361 | ENA |

REPOSITORIES: ENA

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Synapse-centered novel omics targets in Alzheimer’s disease

Project description:Synapse-centered novel omics targets in Alzheimer’s disease

| PRJNA1158813 | ENA

Synapse-centered novel omics targets in Alzheimer’s disease

Project description:Synapse dysfunction is an early event of Alzheimer’s disease (AD). It is caused by multiple cellular and pathological factors such as Amyloid beta, p-tau, inflammation, and aging. However, the exact molecular mechanism of synapse dysfunction in AD is largely unknown. Therefore, to understand the molecular basis of synapse dysfunction in AD, we conducted a high throughput multi-omics analysis of the synaptosome fraction in postmortem brain samples from AD patients and cognitively normal individuals. First, microRNA and mRNA HiSeq analysis were performed on the synaptosomes extracted from the postmortem brains of unaffected control (UC) individuals and AD patients. Next, we conducted the mass spectrometry analysis of synaptosomal proteins in the same sample group of HC and AD. The transcriptomic and proteomic profiling of synaptosome showed the significant deregulation of miRNA, mRNA and protein signatures in AD vs HC. Further, we used an integrated transcriptomic and proteomic approach to understand the molecular interactions of deregulated synapse miRNAs, mRNAs, and proteins in the same samples of AD and HC. Multi-omics integration analysis of synapse miRNAs-mRNAs-proteins revealed the involvement of omics targets in several biological processes and molecular functions such as signal transduction, protein binding, GABAergic synapse, and synaptic vesicle cycle, etc. Our study unveiled synapse-centered novel omics candidates that could be potential therapeutic targets to restore synapse dysfunction in AD.

2025-09-09 | GSE276756 | GEO

Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

2025-09-10 | GSE276898 | GEO

REST targets in the cortex of WT mice and Alzheimer’s disease 3xTg mice

Project description:We profiled REST targets in WT mice, as well as the Alzheimer’s disease 3xTg mouse model, to gain insight into the regulation of physiological pathways by REST, as well as the altered REST cistrome in Alzheimer’s disease.

2022-01-29 | GSE195446 | GEO

Identification of pathological pathways centered on circRNA dysregulation associated with irreversible progression of Alzheimer’s disease [5xFADHippocampus]

Project description:Identification of pathological pathways centered on circRNA dysregulation associated with irreversible progression of Alzheimer’s disease [5xFADHippocampus]

| PRJNA1138662 | ENA

Identification of pathological pathways centered on circRNA dysregulation associated with irreversible progression of Alzheimer’s disease [circGigyf2KD]

Project description:Identification of pathological pathways centered on circRNA dysregulation associated with irreversible progression of Alzheimer’s disease [circGigyf2KD]

| PRJNA1138661 | ENA

Identification of pathological pathways centered on circRNA dysregulation initiated at a critical window of Alzheimer’s disease progression

Project description:Although circRNA abnormalities are found in Alzheimer’s disease (AD) postmortem brains, whether and how altered circRNA landscape lead to pathological gene network changes during AD progression remain undefined. Employing our recently published experimental and computational approaches, we found genome-wide dysregulated circRNA expression and disrupted functional cooperation of circRNAs in sponging microRNAs (miRNAs) and RNA-binding proteins (RBPs) during early pathogenic progression in a mouse AD model. In addition, we identified AD progression-associated mouse circRNAs that are conserved and affected in AD patients, which underlie malfunction of downstream microRNAs and RBPs in AD brains. An exemplar circRNA is circGigyf2, which progressively declines along with AD pathogenic severity. Furthermore, we identified AD pathological pathways centered on circGigyf2, including upstream RBPs that control circGigyf2 biogenesis and downstream miRNA-mRNA and RBP-mRNA axis regulated by circGigyf2, all affected in AD patients. Our discoveries provide strong evidence suggesting the contribution of circRNA abnormality in early AD pathogenesis.

2024-10-22 | GSE236683 | GEO

Expanding the MicroRNA Targeting Code: A Novel Type of Site with Centered Pairing

Project description:We present “centered sites,” a class of microRNA target sites that lacks both perfect seed pairing and 3'-compensatory pairing and instead has 11–12 contiguous Watson–Crick pairs to the center of the microRNA. In elevated Mg2+, centered sites impart mRNA cleavage, but in cells, centered sites repress protein output without consequential Agronaute-catalyzed cleavage. Our study also identified novel extensively paired sites that are cleavage substrates in cultured cells and human brain. This expanded repertoire of cleavage targets and the identification of the centered site type help explain why central regions of many microRNAs are evolutionarily conserved. To study centered sites and identify miRNA cleavage targets, mRNA degradomes were sequenced from human brain and HeLa cells, and smallRNAs were sequenced from human brain and zebrafish embryo at 24 hours post fertilization (hpf). Replicates were combined before the analysis. Fastq files are not available for GSM548638 and GSM548639.

2010-06-25 | E-GEOD-22068 | biostudies-arrayexpress

Synapse to nuclear information transmission by presenilin1-cleavage of PTPRT is undermined in Alzheimer’s disease

Project description:Synapse to nuclear information transmission by presenilin1-cleavage of PTPRT is undermined in Alzheimer’s disease

| PRJNA670928 | ENA

Identification of pathological pathways centered on circRNA dysregulation initiated at a critical window of Alzheimer’s disease progression

Project description:Identification of pathological pathways centered on circRNA dysregulation initiated at a critical window of Alzheimer’s disease progression

| PRJNA992028 | ENA

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