Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Astrocytic tau reduction prevents Ab-induced synaptotoxicity

ABSTRACT: Astrocytic tau reduction prevents Ab-induced synaptotoxicity

PROVIDER: PRJNA823708 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Astrocytic tau reduction prevents Ab-induced synaptotoxicity

Project description:Differential gene expression analysis between WT and TauKO-derived astrocyte cultures

2022-10-12 | GSE200231 | GEO

Astrocytic APOE3-Christchurch expression ameliorates brain amyloid-β pathology in 5xFAD mice

Project description:The rare APOE3-Christchurch (APOE3Ch) variant is linked to resistance against PSEN1 p.E280A-driven autosomal dominant Alzheimer’s disease (AD). Recent studies in AD mouse models have demonstrated an effect of APOE3Ch in reducing tau pathology and tau propagation, yet its effects on amyloid pathology and related toxicity are not fully understood. While prior studies have reported reduced amyloid pathology with APOE3Ch, we extended this knowledge by investigating how astrocyte-specific expression of APOE3Ch impacts amyloid pathology and related responses in 5xFAD mice, an amyloid mouse model. Using adeno-associated virus (AAV)-mediated gene delivery, we overexpressed APOE3 or APOE3Ch in astrocytes of 5xFAD mice at the neonatal stage, then analyzed their effects during the advanced stage of amyloid pathology. Astrocytic APOE expression significantly reduced amyloid burden, neuritic dystrophy, and gliosis compared to GFP controls. Notably, astrocytic APOE3Ch expression, relative to APOE3, markedly lowered oligomeric Ab levels and promoted the formation of more compact, fibrillar plaques, suggesting a shift toward a less toxic aggregation profile. Transcriptomic profiling of cortical tissue revealed broad downregulation of immune-related and proteostatic pathways. These findings indicate that astrocytic APOE3Ch sufficiently attenuates Ab pathology and related toxicity, supporting its potential as a therapeutic modifier for AD.

2026-04-08 | GSE319850 | GEO

The reduction of astrocytic tau prevents amyloid-β-induced synaptotoxicity.

Project description: Not available

| S-EPMC9527666 | biostudies-literature

Inhibition of Astrocytic MAGL Reprograms Glial Reactivity and Prevents Seizure Sequelae

Project description:Inhibition of Astrocytic MAGL Reprograms Glial Reactivity and Prevents Seizure Sequelae

| PRJNA1419241 | ENA

microRNA-132/212 deficiency enhances Ab production and senile plaque deposition in Alzheimer’s disease triple transgenic mice

Project description:The abnormal regulation of amyloid-b (Ab) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimer’s disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Ab deposition and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Ab metabolism, including Tau, Mapk, and Sirt1.

2016-07-17 | GSE84481 | GEO

microRNA-132/212 deficiency enhances Ab production and senile plaque deposition in Alzheimerâs disease triple transgenic mice

Project description:The abnormal regulation of amyloid-b (Ab) metabolism (e.g., production, cleavage, clearance) plays a central role in Alzheimerâs disease (AD). Among endogenous factors believed to participate in AD progression are the small regulatory non-coding microRNAs (miRs). In particular, the miR-132/212 cluster is severely reduced in the AD brain. In previous studies we have shown that miR-132/212 deficiency in mice leads to impaired memory and enhanced Tau pathology as seen in AD patients. Here we demonstrate that the genetic deletion of miR-132/212 promotes Ab deposition and amyloid (senile) plaque formation in triple transgenic AD (3xTg-AD) mice. Using RNA-Seq and bioinformatics, we identified genes of the miR-132/212 network with documented roles in the regulation of Ab metabolism, including Tau, Mapk, and Sirt1. We used RNA-Seq to analyse the hippocampus of 3xTg-AD mice lacking the miR-132/212 cluster as well as Neuro2a cells overexpressing miR-132 mimics.

2016-07-17 | E-GEOD-84481 | biostudies-arrayexpress

Glial profiling of human tauopathy brain demonstrates enrichment of astrocytic transcripts in tau-related frontotemporal degeneration

Project description:To understand how glia may be altered in frontotemporal degeneration with tau pathology (FTD-tau), we used a NanoString glial profiling panel to measure 770 transcripts related to glial biology in human control (n = 8), Alzheimer’s disease (AD) (n = 8), and FTD-tau (n = 8) dorsolateral prefrontal cortex. Compared to control, 43 genes were upregulated and 86 genes were downregulated in the FTD-tau samples. Only 3 genes were upregulated and 2 were downregulated in AD. Pathway analysis revealed many astrocyte-, microglia-, and oligodendrocyte-related pathway scores increased in FTD-tau, while neuron-related pathway scores decreased. We compared these results to a previously published proteomic dataset containing many of the same samples and found that the targeted panel approach obtained measurements for genes whose proteins were not measured in the proteomics. Our results point to the utility of multi-omic approaches and marked dysregulation of glia in FTD-tau.

2022-01-12 | GSE193391 | GEO

Transcriptional vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits

Project description:Alzheimer’s disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral accumulation of amyloid-β (Aβ) and tau, but how memory and emotional neural circuits are disrupted by AD pathology remains unclear. Here, we investigated the transcriptional vulnerability of memory and emotional circuits to concomitant Aβ and tau pathologies in transgenic mice expressing mutant human amyloid precursor protein (APP) and Tau (APP/Tau mice) in excitatory neurons. At 9 months, we detected common and region-specific transcriptional responses in the hippocampus and basolateral amygdala (BLA) of APP/Tau mice, including astrocytic, microglia and 63 AD-associated genes. These findings suggest that Aβ and tau pathologies disrupt region-specific gene expression programs underlying vulnerability of memory and emotional circuits to AD neuropathology.

2025-02-07 | GSE279050 | GEO

Axonal tau reduction ameliorates tau and amyloid pathology in a mouse model of Alzheimer’s disease

Project description:Pathological deposition of hyperphosphorylated tau in the brain closely correlates with the course of Alzheimer´s disease (AD). Tau pathology occurs first in axons of affected neurons and tau removal from axons might thus be an early intervention strategy. We report that the RNA-binding protein hnRNP R facilitates the axonal localization of the Mapt mRNA encoding tau. Mapt mRNA and tau protein were reduced in axons but not cell bodies of primary neurons cultured from hnRNP R knockout mice. Brains of 5xFAD mice deficient for hnRNP R contained less phospho-tau aggregates and amyloid-β plaques in cortex and hippocampus. Treatment of neurons with antisense oligonucleotides (MAPT-ASOs) to block hnRNP R binding to Mapt similarly reduced axonal tau levels, and intracerebroventricular injection of a MAPT-ASO ameliorated the phospho-tau and plaque load in 5xFAD mice. Lowering of tau selectively in axons thus represents an innovative therapeutic perspective for treatment of AD and other tauopathies.

2025-08-04 | PXD053387 | Pride

Glial profiling of human tauopathy brain demonstrates enrichment of astrocytic transcripts in tau-related frontotemporal degeneration

Project description:Glial profiling of human tauopathy brain demonstrates enrichment of astrocytic transcripts in tau-related frontotemporal degeneration

| PRJNA796018 | ENA

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