Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down syndrome.

ABSTRACT: Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down syndrome.

PROVIDER: PRJNA573911 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10174271.fastq.gz	Fastqsanger.gz
	SRR10174272.fastq.gz	Fastqsanger.gz
	SRR10174273.fastq.gz	Fastqsanger.gz
	SRR10174274.fastq.gz	Fastqsanger.gz
	SRR10174275.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down Syndrome.

Project description:Microglia are the resident immune cells of the brain and have been implicated in mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by the presence of a supernumerary chromosome 21, which contains genes essential for the function of the immune system. Here, we investigated the presence of microglial alterations and their implication for cognitive impairment in the Dp(16) mouse model of DS. In the hippocampus of Dp(16) mice and individuals with DS, we found microglial morphology indicative of an activated state. Accordingly, we found increased levels of pro-inflammatory cytokines and altered interferon signaling in Dp(16) mice. In addition, Dp(16) mice showed decreased dendritic spine density and cognitive deficits. Remarkably, depletion of defective microglia by PLX3397 treatment or rescue of the microglia activated state by the commonly used anti-inflammatory drug acetaminophen fully rescued dendritic-spine density and cognitive deficits in Dp(16) mice. Our data suggest an involvement of microglia in the cognitive impairment of DS animals and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

2020-09-22 | PXD015113 | Pride

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down Syndrome.

2020-09-22 | PXD015148 | Pride

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down syndrome.

Project description:Microglia are the resident immune cells of the brain and have been implicated in mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by the presence of a supernumerary chromosome 21, which contains genes essential for the function of the immune system. Here, we investigated the presence of microglial alterations and their implication for cognitive impairment in the Dp(16) mouse model of DS. In the hippocampus of Dp(16) mice and individuals with DS, we found microglial morphology indicative of an activated state. Accordingly, we found an electrophysiological profile typical of activated microglia, increased levels of pro-inflammatory cytokines, and altered interferon signaling in Dp(16) mice. In addition, DS mice showed decreased neuronal spine density and neuronal activity, as well as cognitive behavioral deficits. Remarkably, depletion of defective microglia by PLX3397 treatment or rescue of the microglia activated state by the commonly used anti-inflammatory drug acetaminophen rescued the neuronal deficits and cognitive impairment in Dp(16) mice. Our data suggest an involvement of microglia in the cognitive impairment of DS animals and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

2020-09-22 | GSE137939 | GEO

Rescuing Over-activated Microglia Restores Cognitive Performance in Juvenile Animals of the Dp(16) Mouse Model of Down Syndrome.

Project description:Microglia are brain-resident immune cells and regulate mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by a supernumerary chromosome 21, containing also genes related to the immune system. In the hippocampus of the Dp(16) mouse model of DS and DS individuals, we found activated microglia, as assessed by their morphology; activation markers; and, for DS mice, electrophysiological profile. Accordingly, we found increased pro-inflammatory cytokine levels and altered interferon signaling in Dp(16) hippocampi. DS mice also showed decreased spine density and activity of hippocampal neurons and hippocampus-dependent cognitive behavioral deficits. Depletion of defective microglia or treatment with a commonly used anti-inflammatory drug rescued the neuronal spine and activity impairments and cognitive deficits in juvenile Dp(16) mice. Our results suggest an involvement of microglia in Dp(16)-mouse cognitive deficits and identify a new potential therapeutic approach for cognitive disabilities in DS individuals.

| S-EPMC7736620 | biostudies-literature

Acetaminophen

Project description:Acetaminophen

| PRJNA629821 | ENA

Diplodia sp. Dp 5 strain:Dp 5

Project description:Diplodia sp. Dp 5 transcriptome - Dp 5-B.2

| PRJNA584235 | ENA

Diplodia sp. Dp 3 strain:Dp 3

Project description:Diplodia sp. Dp 3 transcriptome - Dp 3-C.2

| PRJNA584038 | ENA

Acetaminophen

Project description:8 and 80 week old mice treated with acetaminophen