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The microglial transcriptome of a novel murine model of Alzheimer's Disease: phagocytically active and inactive microglia from homozygous App-SAA mice and WT littermate controls.

ABSTRACT: The microglial transcriptome of a novel murine model of Alzheimer's Disease: phagocytically active and inactive microglia from homozygous App-SAA mice and WT littermate controls.

PROVIDER: PRJNA664126 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12661500.fastq.gz	Fastqsanger.gz
	SRR12661501.fastq.gz	Fastqsanger.gz
	SRR12661502.fastq.gz	Fastqsanger.gz
	SRR12661503.fastq.gz	Fastqsanger.gz
	SRR12661504.fastq.gz	Fastqsanger.gz

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The microglial transcriptome of a novel murine model of Alzheimer's Disease: FACS-isolated microglia from heterozygous and homozygous App-SAA mice and WT littermate controls.

Project description:We created a novel murine model of Alzheimer's Disease using a knock-in strategy to humanize the sequence of the murine App gene and introduced three familial AD (FAD) mutations, Swedish (Swedish (KM670/671NL), Arctic (E693G)) and Austrian (T712I). We characterized the effects of these genetic modifications on the transcriptome of FACS-isolated microglia from 8-month-old App-SAA mice. Numerous genes were differentially expressed between cells from homozygous App-SAA animals compared to those from WT littermates. For example, we observed up-regulation of Disease-associated microglia (DAM) genes. In contrast, the transcriptome of microglia from heterozygous App-SAA animals broadly resembles that of their WT counterparts.

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The microglial transcriptome of a novel murine model of Alzheimer's Disease: phagocytically active and inactive microglia from homozygous App-SAA mice and WT littermate controls.

Project description:We created a novel murine model of Alzheimer's Disease using a knock-in strategy to humanize the sequence of the murine App gene and introduced three familial AD (FAD) mutations, Swedish (Swedish (KM670/671NL), Arctic (E693G)) and Austrian (T712I). To determine whether App-SAA microglia exhibit cellular dysfunctions and whether these dysfunctions relate to fibrillar Ab internalization, mice were intraperitoneally (i.p.) injected with 10 mg/kg methoxy-X04. 24 hours after injection, mice were perfused with PBS, cortical and hippocampal tissues were dissected and processed into single-cell suspension and methoxy-X04-negative and methoxy-X04-positive microglia were isolated using FACS. Mirroring our gene expression studies, we found profound alterations of the AppSAA microglia transcriptome; these changes were exacerbated in methoxy-X04 positive compared to negative cells.

2021-01-20 | GSE158153 | GEO

The microglial transcriptome of a novel murine model of Alzheimer's Disease: FACS-isolated microglia from heterozygous and homozygous App-SAA mice and WT littermate controls.

Project description:The microglial transcriptome of a novel murine model of Alzheimer's Disease: FACS-isolated microglia from heterozygous and homozygous App-SAA mice and WT littermate controls.

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Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.

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Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.

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Project description:Amyloid precursor protein (APP) is associated with both familial and sporadic forms of Alzheimer’s disease. APP has two homologs, amyloid precursor-like protein 1 and 2 (APLP1 and APLP2), and they have functional redundancy. APP intracellular c-terminal domain (AICD), produced by sequential α- or β- and γ-secretase cleavages, is thought to control gene expression, similarly as the ICD of Notch. To investigate the role of APP family in transcriptional regulation, we examined gene expression changes in the cerebral cortex of APP/APLP1/APLP2 conditional triple knockout (cTKO) mice, in which APP family members are selectively inactivated in excitatory neurons of the postnatal forebrain. Of the 12 previously reported AICD target genes, only Nep and Npas4 mRNA levels were significantly reduced in the cerebral cortex of cTKO mice, compared to littermate controls. We further examined global transcriptional changes by RNA-seq and identified 189 and 274 differentially expressed genes in the neocortex and hippocampus, respectively, of cTKO mice relative to controls. Gene Ontology analysis indicated that these genes are involved in a variety of cellular functions, including extracellular organization, learning and memory, and ion channels. Thus, inactivation of APP family alters transcriptional profiles of the cerebral cortex and affects wide-ranging molecular pathways.

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Lysosomal dysfunction in Down syndrome is APP-dependent and mediated by APP-βCTF (C99)

Project description:Lysosomal failure underlies pathogenesis of numerous congenital neurodegenerative disorders and is an early and progressive feature of Alzheimer’s disease (AD) pathogenesis. Here, we report that lysosomal dysfunction in Down Syndrome (Trisomy 21) requires the extra gene copy of amyloid precursor protein (APP) and is mediated by the beta cleaved carboxy terminal fragment of APP (APP-βCTF, C99). In primary fibroblasts from individuals with Down Syndrome (DS), lysosomal degradation of autophagic and endocytic substrates is selectively impaired causing them to accumulate in enlarged autolysosomes/lysosomes. Direct measurements of lysosomal pH uncovered a significant elevation (0.6 units) associated with slowed LC3 turnover and the inactivation of cathepsin D (CTSD) and other lysosomal hydrolases known to be unstable or less active when lysosomal pH is persistently elevated. RNA sequencing analysis excluded a transcriptional contribution to hydrolase declines. Normalizing lysosome pH by delivering acidic nanoparticles to lysosomes ameliorated lysosomal deficits, implicating pH elevation as their primary basis. Cortical neurons cultured from the Ts2 mouse model of DS exhibited lysosomal deficits similar to those in DS cells. Lowering APP expression with siRNA or BACE1 inhibition reversed cathepsin deficits in both fibroblasts and neurons. Deleting one BACE1 allele from adult Ts2 mice had similar rescue effects in vivo. The modest elevation of endogenous APP-βCTF needed to disrupt lysosomal function in DS is relevant to sporadic AD where APP-βCTF, but not APP, is also elevated. Our results extend evidence that impaired lysosomal acidification drives progressive lysosomal failure in multiple forms of AD.

2019-05-30 | GSE127880 | GEO

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