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Single nucleus RNA sequencing of the cortex of antibiotic and vehicle treated APPPS1-21 mice

ABSTRACT: Single nucleus RNA sequencing of the cortex of antibiotic and vehicle treated APPPS1-21 mice

PROVIDER: PRJNA1254715 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33292111.fastq.gz	Fastqsanger.gz
	SRR33292112.fastq.gz	Fastqsanger.gz
	SRR33292113.fastq.gz	Fastqsanger.gz
	SRR33292114.fastq.gz	Fastqsanger.gz
	SRR33292115.fastq.gz	Fastqsanger.gz

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Single nucleus RNA sequencing of the cortex of antibiotic and vehicle treated APPPS1-21 mice

Project description:Previously, we and others have shown that broad spectrum antibiotic treatment from postnatal day 14-21 reduces neuroinflammation in the APPPS1-21 model of AD-related amyloidosis. In the current study, we used single-nucleus RNA sequencing (snRNAseq) to assess cell-type specific transcriptional changes in antibiotic treated mice and controls. We also assessed changes in astrocyte subclusters in these groups.

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Project description:Previously, we have shown that broad spectrum antibiotic treatment reduces reactive astrocyte phenotypes in the APPPS1-21 model of AD-related amyloidosis. We have also found that antibiotics selectively increases propionate levels and exogenous propionate treatment recapitulates phenotypes observed in antibiotic treated mice. In the current study, we wanted to assess astrocyte transcriptional state using bulk RNA sequencing. To accomplish this we used translating ribosome affinity purification (TRAP) sequencing, a ribosomal protein L10a is fused to eGFP under the control of a cell type specific promoter in a transgenic mouse model. We crossed APPPS1-21 mice to the Aldh1l1-eGFP/Rpl10a bacTRAP mouse model and progeny were treated with antibiotics, propionate, or VHL and performed bulk TRAPseq.

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RNAseq of cortex of 6-month old APPPS1 and APPPS1;Apoe-/- mice

Project description:One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. ApoE influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1∆E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology.

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