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A single-nucleus transcriptomic atlas reveals cellular and genetic characteristics in the hippocampus of natural aging-inducing Alzheimer’s disease tree shrews

ABSTRACT: A single-nucleus transcriptomic atlas reveals cellular and genetic characteristics in the hippocampus of natural aging-inducing Alzheimer’s disease tree shrews

PROVIDER: PRJNA987690 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25031536_1.fastq.gz	Fastqsanger.gz
	SRR25031536_2.fastq.gz	Fastqsanger.gz
	SRR25031537_1.fastq.gz	Fastqsanger.gz
	SRR25031537_2.fastq.gz	Fastqsanger.gz
	SRR25031538_1.fastq.gz	Fastqsanger.gz

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A single-nucleus transcriptomic atlas reveals cellular and genetic characteristics in the hippocampus of natural aging-inducing Alzheimer’s disease tree shrews

Project description:Natural aging-inducing Alzheimer’s disease (AD) model is lacking in the current preclinical research. Here, we surprisingly screened 10 tree shrews (TS) with obvious AD phenotypes from 324 naturally aging TS. Using single-nucleus RNA sequencing, we generated the transcriptome atlas of cellular and genetic diversity underlying natural aging-inducing AD development in TS. Further analyses and immunostaining verified the larger proportion of citatory neuronal progenitors exhibiting two different trajectories to an excitatory neuron subtype and granule cells with higher AD relevance. The intensified cellular communication was also found between progenitors and oligodendrocytes. Intriguingly, cross-species analysis among human, TS, monkeys, and mice delineated the cellular heterogeneity and further confirmed higher similarities of TS to monkeys than mice. Overall, our study established the first single-nucleus transcriptomic atlas of hippocampus in a novel AD model, extending our understanding of progenitors in the natural aging processes, and providing striking reference for diagnosis and treatment of AD.

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Evaluation And Characterization Of Acute Respiratory Distress Syndrome In Tree Shrews Through TMT Proteomic Method

Project description:Acute respiratory distress syndrome (ARDS), a common cause of acute fatal respiratory, is characterized by severe inflammatory lung injury as well as hallmarks of increased pulmonary vascular permeability, neutrophil infiltration, and macrophage accumulation. Tree shrew, a squirrel-like small animal model, has been confirmed more similar traits to human ARDS with one-hit intratracheal instillation of LPS in our previous study. In this study, we characterized protein profile changes induced by intranasal LPS challenge in the tree shrew model through tandem mass tag (TMT)-based quantitative proteomics and type II alveolar epithelial cells through pathological analysis. In total, 4070 proteins (p < 0.05) were identified from lung tissues of the LPS-induced group and PBS group. Among the differential expression proteins (DEPs) detected by t-test (≥|1.5-fold|), 529 DEPs were identified, of which 304 were upregulated, and 225 were downregulated. The most important pathways involved in the process of ARDS had been identified by enrichment analysis: oxidative stress, apoptosis, inflammatory responses, and vascular endothelial injury. In addition, proteins have been reported in animal models or clinical patients also detail investigated for further analysis, such as ceruloplasmin (CP), hemopexin (HPX), sphingosine kinase 1 (SphK1), lactotransferrin (LTF), and myeloperoxidase (MPO) were upregulated in induced tissues and confirmed by western blot analysis. Overall, this study not only reveals a comprehensive proteomic analysis of the ARDS tree shrew model but also provides novel insights into multi-pathways responses induced by the LPS challenge of tree shrews. We highlight shared and unique proteomic changes in the lungs of ARDS tree shrews and identify novel pathways for acute lung injury, which may promote the model into basic research and translational research.

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Project description:Microglia is dynamically reprogrammed according to the progression of Alzheimer’s disease (AD). However, clinical translation into biomarker development for functional change in microglia has not been achieved. Here, we find the close association of the metabolic reconfiguration of microglia with increased hippocampal glucose uptake, which can be noninvasively estimated by [18F]fluorodeoxyglucose (FDG) positron emission tomography (PET). We found that increased FDG activity in the hippocampus of an AD mouse model depended on microglial uptake. Single-cell RNA-sequencing of the hippocampus showed the changes of glucose metabolism profiles including glucose transporters, glycolysis and oxidative phosphorylation mainly occurred in microglia. A subset of microglia with high glucose transporters with defective glycolysis and oxidative phosphorylation was increased according to disease progression. Furthermore, we also found a positive association between a soluble TREM2 of cerebrospinal fluid, a marker of microglial activation, and hippocampal FDG uptake as a human study. We identified a reconfiguration of microglial glucose metabolism in the hippocampus of AD and suggested a feasible imaging biomarker based on widely used FDG PET to reflect microglial metabolic profiles.

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