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Drosophila melanogaster

ABSTRACT: Molecular and Pathological Interactions among Aβ42, Tau, TREM2, and TYROBP in Drosophila Models

PROVIDER: PRJNA386996 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5572730.fastq.gz	Fastqsanger.gz
	SRR5572740.fastq.gz	Fastqsanger.gz
	SRR5572750.fastq.gz	Fastqsanger.gz
	SRR5572760.fastq.gz	Fastqsanger.gz
	SRR5572731.fastq.gz	Fastqsanger.gz

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Molecular and Pathological Interactions among Aβ42, Tau, TREM2, and TYROBP in Drosophila Models

Project description:Cerebral amyloidosis, neuroinflammation, and tauopathy are key features of Alzheimer’s disease (AD), but interactions among these features remain poorly understood. Our previous multiscale molecular network models of AD revealed TYROBP as a key driver of an immune- and microglia-specific network that was robustly associated with AD pathophysiology. Recent genetic studies of AD further identified pathogenic mutations in both TREM2 and TYROBP. In this study, we systematically examined molecular and pathological interactions among Aβ, tau, TREM2 and TYROBP by integrating signatures from transgenic Drosophila models of AD and transcriptome-wide gene co-expression networks from two human AD cohorts.

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Project description:Loss-of-function mutations in TREM2 (triggering receptor expressed on myeloid cells 2) strongly increase Alzheimer’s disease (AD) risk. Preclinical models using Trem2 deletion or overexpression have revealed a protective Trem2 function related to β-amyloid accumulation, a process that is most prominent during the pre-diagnosis stages of AD. The role of TREM2 in later AD stages characterized by tau-mediated neurodegeneration is less clear. To understand Trem2 function in the context of both β-amyloid and tau pathologies, we examined Trem2-deficient mice expressing mutant tau alone (pR5-183 model) or in the TauPS2APP model, in which β-amyloid pathology exacerbates tau pathology and neurodegeneration. Single-cell RNA-sequencing in these models revealed robust disease-associated microglia (DAM) activation in TauPS2APP mice that was both amyloid-dependent and Trem2-dependent. In the presence of β-amyloid pathology, Trem2 deletion further exacerbated tau accumulation and spreading and promoted brain atrophy. Without β-amyloid pathology, Trem2 deletion did not affect these processes. Therefore, TREM2 may slow AD progression and reduce tau-driven neurodegeneration by restricting the degree to which β-amyloid facilitates the spreading of pathogenic tau

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