Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of different miRNAs in Alzheimer's disease and vascular cognitive impairment and dementia

ABSTRACT: Identification of different miRNAs in Alzheimer's disease and vascular cognitive impairment and dementia

PROVIDER: PRJNA904393 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22383500.fastq.gz	Fastqsanger.gz
	SRR22383501.fastq.gz	Fastqsanger.gz
	SRR22383502.fastq.gz	Fastqsanger.gz
	SRR22383503.fastq.gz	Fastqsanger.gz
	SRR22383504.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Identification of different miRNAs in Alzheimer's disease and vascular cognitive impairment and dementia

Project description:There are many subtypes of dementia without any minimally invasive, low-cost and efficient diagnostic biomarkers. MicroRNA (miRNA) are easily gained and accessible from patients, which may be a promising biomarker for dementia diagnosis and differential diagnosis. We make a completely expression analysis of serum miRNA from 24 participants including post-stroke cognitive impairment (PSCI) group (n=6), post-stroke non-cognitive impairment (PSCI) group, Alzheimer's Disease (AD) group (n=6) and normal control group (NC) group (n=6). Different expression miRNA (DE -miRNA) were screened by LIMMA ebayes method, Benjamini-Hochberg check and fold change (P < 0.05, |log2FC|≥1), we construct a DE-miRNA-key gene-signaling pathway network, the roles of DE-miRNA and related genes and signaling pathways in AD and PSCI were deduced through comprehensive network construction and literature search.

2024-04-17 | GSE218605 | GEO

microRNA microarray profile in the plasma of mild cognitive impairment due to Alzheimer's disease

Project description:To explore the microRNAs associated with pathology of early Alzheimer's disease, we detected the microRNA profiles in the plasma of subjects with mild cognitive impairment due to Alzheimer's disease and gender-, age-, education-matched normal control elderly.

2020-03-20 | GSE147232 | GEO

Long noncoding RNA microarray profile in the plasma of mild cognitive impairment due to Alzheimer's disease

Project description:To explore the lncRNAs associated with pathology of early Alzheimer's disease, we detected the lncRNA profiles in the plasma of subjects with mild cognitive impairment due to Alzheimer's disease and gender-, age-, education-matched normal control elderly.

2023-03-01 | GSE225304 | GEO

Intermittent Fasting Reprograms the Brain Proteome to Prevent Synaptic Degeneration and Cognitive Impairment in Vascular Dementia

Project description:Vascular dementia (VaD), driven by chronic cerebral hypoperfusion (CCH), leads to synaptic degeneration and cognitive decline, yet mechanisms linking vascular dysfunction to synaptic loss remain unclear. Intermittent fasting (IF) has emerged as a potential intervention, but its effects on synaptic integrity in VaD are unknown. Using the bilateral common carotid artery stenosis (BCAS) mouse model, we demonstrate that a 16-hour IF regimen preserves cognitive function and cortical synaptic density despite persistent hypoperfusion. Behavioral assays revealed that IF prevented spatial memory deficits in BCAS mice, while electron microscopy confirmed synaptic preservation without altering baseline architecture. Surprisingly, synaptic protein levels remained unchanged, suggesting IF protects synaptic function rather than abundance. Proteomic profiling uncovered dynamic hippocampal adaptations under IF, including upregulation of synaptic stabilizers, enhanced GABAergic signaling, and suppression of neuroinflammatory mediators. IF also attenuated microglial engulfment of synapses, indicating modulation of complement-mediated pruning. Temporal pathway analysis revealed IF’s multi-phase neuroprotection: early synaptic reinforcement, mid-phase metabolic optimization, and late-phase suppression of chronic neuroinflammation. These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. Our results highlight IF’s potential as a non-pharmacological strategy to combat vascular cognitive impairment by targeting the synaptic vulnerability underlying dementia progression.

2025-09-08 | PXD064537 | Pride

Alzheimer, Mild Cognitive impairment and control samples from AddneuroMed Cohort (batch 2)

Project description:Alzheimer case-control samples originate from the EU funded AddNeuroMed Cohort, which is a large cross-European AD biomarker study relying on human blood as the source of RNA. The design is case-control. Cases are either Alzheimer's disease patients, subjects with mild cognitive impairment or age and gender matched controls.

2015-08-05 | E-GEOD-63061 | biostudies-arrayexpress

Multi-Omics Integration Implicates Rac/Rho GTPase Cycling in Vascular Cognitive Impairment and Dementia Pathogenesis

Project description:Background: Vascular cognitive impairment and dementia (VCID) represents a spectrum of cognitive disorders linked to cerebrovascular pathology, yet its molecular underpinnings remain misunderstood. Methods: We conducted a multi-omics analysis of post-mortem brain tissue from the superior parietal lobe (Brodmann area 7) in 19 individuals with neuropathologically confirmed VCID and 21 age-matched controls. Whole genome sequencing, genome-wide DNA methylation profiling, transcriptomic analysis, and metabolomics profiling were performed to identify molecular signatures and integrated pathways involved in VCID pathogenesis. Results: Epigenome-wide association analysis revealed widespread hypermethylation in VCID, with significant enrichment of genes involved in the Rac/Rho GTPase cycle and cytoskeletal remodeling. Transcriptomic analysis confirmed dysregulation of small GTPase signaling, oxidative stress responses, and lipid metabolism. Metabolomic profiling identified altered levels of diacylglycerols (DAGs) and phosphatidylethanolamines (PEs), which showed strengthened associations with Rac/Rho pathway genes in VCID compared to controls. Conclusions: Our integrative multi-omics study identifies the Rac/Rho GTPase cycle as a convergent pathway disrupted at the genomic, epigenomic, transcriptomic, and metabolic levels in VCID. Lipid metabolism, particularly involving DAGs and PEs, emerged as a key downstream effector contributing to VCID. These findings offer mechanistic insights into VCID pathogenesis and suggest lipid signaling pathways as promising therapeutic targets for intervention.

2025-07-28 | GSE303449 | GEO

Ginsenoside CK improves cognitive impairment

Project description:Alzheimer's disease (AD) is a neurodegenerative disease and is the most common form of dementia, cognitive dysfunction is a pre-AD manifestation, followed by progressive deterioration in behavior and mood, CK has good pharmacological activity, inhibit neuronal damage associated with Aβ and improve learning memory in mice through its antioxidative properties. We used microarrays to detail the regulation of brain tissue genes in cognitively impaired mice by ginsenoside CK.

2023-02-10 | GSE221791 | GEO

Multi-Omics Integration Implicates Rac/Rho GTPase Cycling in Vascular Cognitive Impairment and Dementia Pathogenesis

Project description:Multi-Omics Integration Implicates Rac/Rho GTPase Cycling in Vascular Cognitive Impairment and Dementia Pathogenesis

| PRJNA1295451 | ENA

Sex-dependent APOE4 Neutrophil-microglia interactions drive cognitive impairment in Alzheimer's Disease

Project description:APOE4 is the strongest genetic risk factor for Alzheimer's disease (AD) with increased odds ratios in females. Targeting amyloid plaques show modest improvement in male non-APOE4 carriers. Leveraging single cell transcriptomics across APOE variants in both sexes, multiplex flow cytometry and validation in two independent cohorts of APOE4 female AD patients, we identify a new subset of neutrophils, interacting with microglia associated with cognitive impairment. This phenotype is defined by increased IL-17 and IL-1 co-expressed gene modules in blood neutrophils and in microglia of cognitively impaired female APOE e4 carriers, showing increased infiltration to the AD brain. APOE4 female IL-17+ neutrophils upregulated the immunosuppressive cytokines IL-10 and TGFb, and immune checkpoints including LAG-3 and PD-1, associated with accelerated immune aging. Deletion of APOE4 in neutrophils reduced this immunosuppressive phenotype and restored microglial response to neurodegeneration (MGnD), limiting plaque pathology in AD mice. Mechanistically, IL-17F upregulated in APOE4 neutrophils interacts with microglial IL-17RA to suppress the induction of MGnD phenotype, and blocking this axis supported cognitive improvement in AD mice. These findings provide a translational basis to target IL-17F in APOE e4 female carriers with cognitive impairment.

2024-06-04 | GSE262632 | GEO

Sex-dependent APOE4 Neutrophil-microglia interactions drive cognitive impairment in Alzheimer's Disease

Project description:APOE4 is the strongest genetic risk factor for Alzheimer's disease (AD), with increased odds ratios in females. Targeting amyloid plaques shows modest improvement in male non-APOE4 carriers. Leveraging single-cell transcriptomics across APOE variants in both sexes, multiplex flow cytometry, and validation in two independent cohorts of APOE4 female AD patients, we identify a new subset of neutrophils interacting with microglia associated with cognitive impairment. This phenotype is defined by increased IL-17 and IL-1 co-expressed gene modules in blood neutrophils and in microglia of cognitively impaired female APOE e4 carriers, showing increased infiltration to the AD brain. APOE4 female IL-17+ neutrophils upregulated the immunosuppressive cytokines IL-10 and TGFB and immune checkpoints, including LAG-3 and PD-1, associated with accelerated immune aging. Deletion of APOE4 in neutrophils reduced this immunosuppressive phenotype and restored the microglial response to neurodegeneration (MGnD), limiting plaque pathology in AD mice. Mechanistically, IL-17F upregulated in APOE4 neutrophils interacts with microglial IL-17RA to suppress the induction of MGnD phenotype, and blocking this axis supported cognitive improvement in AD mice. These findings provide a translational basis to target IL-17F in APOE e4 female carriers with cognitive impairment.

2024-06-04 | GSE260461 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data