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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo

ABSTRACT: Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo

PROVIDER: PRJNA665285 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12608405_1.fastq.gz	Fastqsanger.gz
	SRR12608405_2.fastq.gz	Fastqsanger.gz
	SRR12608406_1.fastq.gz	Fastqsanger.gz
	SRR12608406_2.fastq.gz	Fastqsanger.gz
	SRR12608407_1.fastq.gz	Fastqsanger.gz

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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [scRNA-seq]

Project description:Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [scRNA-seq]

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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [bulk RNA-seq]

Project description:Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [bulk RNA-seq]

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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [scRNA-seq]

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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer’s pathology in vivo [RNA-seq]

Project description:Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer’s pathology in vivo [RNA-seq]

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Expression data from WT and TREM2 deficient microglia in a mouse model of Alzheimer's disease

Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease Microglia were FACS-purified from 8.5 month old WT, Trem2-/-, 5XFAD, and Trem2-/- 5XFAD mice

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TREM2 haploinsufficiency impairs microglia’s response to injury and exacerbates tau pathology in a tauopathy mouse model [RNA-Seq]

Project description:Alzheimer's disease (AD), the most common form of dementia, is characterized by the abnormal accumulation of amyloid plaques and hyperphosphorylated tau aggregates, as well as microgliosis. The link between mutations in Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), a microglia-expressed gene, and the increased risk for developing late-onset AD suggests a detrimental role for microglia in disease pathophyioslogy. Hemizygous TREM2 mutations are posited to increase risk for AD through loss-of-function haploinsufficiency. The effects of TREM2 haploinsufficiency on tau pathology and tau-associated deficits have not yet been characterized. Using in vivo imaging, we showed that TREM2 haploinsufficiency, but not complete loss of TREM2, resulted in a striking agedependent impairment in microglia’s response to injury without affecting baseline motility. This TREM2-dependent effect on microglial motility is consistent with transcriptomic alterations in cell motility uncovered with unbiased RNAsequencing analysis. Moreover, TREM2 haploinsufficiency, but not complete loss of TREM2, exacerbated phosphorylated tau pathology in transgenic mice expressing mutant human tau. In addition, TREM2 haploinsufficiency increased tau inclusions and tau-mediated inflammation without further exacerbating neuronal loss. Our findings demonstrate for the first time that TREM2 haploinsufficiency induces deficits in a tauopathy mouse model, supporting the notion that the hemizygous missense variant results in loss-of-function.

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Transcriptomic and functional deficits in human TREM2-/- microglia impair response to Alzheimer's pathology in vivo [bulk RNA-seq]

Project description:Bulk RNA sequencing data comparing TREM2 WT and KO microglia responses to treatment with dead neurons.

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Project description:CD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer’s disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33.

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TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease

Project description:TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease

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Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer's Disease model

Project description:TREM2 is a receptor for lipids expressed in microglia. The R47H variant of human TREM2 impairs ligand binding and increases Alzheimer’s Disease (AD) risk. In mouse models of amyloid b (Ab) accumulation, defective TREM2 function affects microglial response to Ab plaques exacerbating tissue damage, whereas TREM2 overexpression attenuates pathology. Thus, AD may benefit from TREM2 activation. Here, we examined the impact of an anti-human TREM2 agonistic mAb, AL002c, in a mouse AD model expressing either the common variant (CV) or the R47H variant of TREM2. Single cell RNA-seq of microglia after acute systemic administration of AL002c showed induction of proliferation in both CV- and R47H-transgenic mice. Prolonged administration of AL002c reduced filamentous plaques and neurite dystrophy, impacted behavior and tempered glial inflammatory response. We further showed that a variant of AL002c has been given safely in a first-in-human phase I clinical trial and engages TREM2 based on CSF biomarkers. We conclude that AL002c is a promising candidate for AD therapy.

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