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Synapse to nuclear information transmission by presenilin1-cleavage of PTPRT is undermined in Alzheimer’s disease

ABSTRACT: Synapse to nuclear information transmission by presenilin1-cleavage of PTPRT is undermined in Alzheimer’s disease

PROVIDER: PRJNA670928 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12884157_1.fastq.gz	Fastqsanger.gz
	SRR12884157_2.fastq.gz	Fastqsanger.gz
	SRR12884158_1.fastq.gz	Fastqsanger.gz
	SRR12884158_2.fastq.gz	Fastqsanger.gz
	SRR12884159_1.fastq.gz	Fastqsanger.gz

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Synapse to nuclear information transmission by presenilin1-cleavage of PTPRT is undermined in Alzheimer’s disease

Project description:PTPRT (receptor-type tyrosine-protein phosphatase T), as a brain-specific type 1 transmembrane protein, plays important function in neurodevelopment and synapse formation. Here, we report that the downregulated levels of Ptprt mRNA and protein is found in both human AD and APP/PS1 mouse brains. We further identified that PTPRT intracellular domain (ICD), which was released by ADAM10- and g-secretase-dependent cleavage of PTPRT, efficiently translocated to the nucleus via a conserved nuclear localization signal. RNA sequencing reveals that expression of the PICD alone can profoundly alter the expression of genes associated with synapse function and dephosphorylation, phosphatase and cell adhesion. Inhibition of nuclear-localization of PICD via the mutation of its nuclear localization signal (NLS) leads to accumulation of phosphorylated signal transducer and activator of transcription 3 (p-STAT3), which is a substrate of PTPRT and eventually resulted in neuronal cell death. AVV1-PICD in vitro and in vivo robustly decreases the levels of phosph-STAT3(Y705) in APP/PS1 neurons, attenuates Ab pathology, and improves synaptic function and behavioral deficits in APP/PS1 mice. Our findings define a novel role of decreased PTPRT and its nuclear ICD fragment in the events promote AD pathogenesis.

2022-10-23 | GSE159943 | GEO

Synapse-centered novel omics targets in Alzheimer’s disease

Project description:Synapse-centered novel omics targets in Alzheimer’s disease

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Synapse-centered novel omics targets in Alzheimer’s disease

Project description:Synapse dysfunction is an early event of Alzheimer’s disease (AD). It is caused by multiple cellular and pathological factors such as Amyloid beta, p-tau, inflammation, and aging. However, the exact molecular mechanism of synapse dysfunction in AD is largely unknown. Therefore, to understand the molecular basis of synapse dysfunction in AD, we conducted a high throughput multi-omics analysis of the synaptosome fraction in postmortem brain samples from AD patients and cognitively normal individuals. First, microRNA and mRNA HiSeq analysis were performed on the synaptosomes extracted from the postmortem brains of unaffected control (UC) individuals and AD patients. Next, we conducted the mass spectrometry analysis of synaptosomal proteins in the same sample group of HC and AD. The transcriptomic and proteomic profiling of synaptosome showed the significant deregulation of miRNA, mRNA and protein signatures in AD vs HC. Further, we used an integrated transcriptomic and proteomic approach to understand the molecular interactions of deregulated synapse miRNAs, mRNAs, and proteins in the same samples of AD and HC. Multi-omics integration analysis of synapse miRNAs-mRNAs-proteins revealed the involvement of omics targets in several biological processes and molecular functions such as signal transduction, protein binding, GABAergic synapse, and synaptic vesicle cycle, etc. Our study unveiled synapse-centered novel omics candidates that could be potential therapeutic targets to restore synapse dysfunction in AD.

2025-09-09 | GSE276756 | GEO

Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

2025-09-10 | GSE276898 | GEO

Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

Project description:Synapse-centered novel omics targets in Alzheimer’s disease - miRNA

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Protein local synthesis at synapse is required for neuromuscular transmission

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Single-cell transcriptome depicts the molecular dynamics of synapse formation in mouse hippocampus

Project description:Synapses are asymmetric junctions between presynaptic and postsynaptic neurons that mediate information transfer in the brain. The proper formation of functional synapses is crucial for synaptic transmission and brain function. However, how neurons initially recognize each other to form synapses remain to be elucidated. Here, we performed single-cell RNA sequencing of the cultured hippocampal cells on the critical time points during synapse development. . We first built comprehensive single-cell transcriptomic atlas of hippocampus undergoing synapse formation. Furthermore, we focused on neurons, and systematically analyzed temporal dynamic functional transcription factors hubs.. We identified that transcription factors, such as EGR family genes, AP-1 family genes, NeuroD family genes, NF1 family genes, may act as key regulators of synapse formation. Besides, we provided the resources of increased membrane and secretory proteins associated with synapse formation, which including previously reported synapse formation genes, Nlgn3, Nectin1, Dag1, Snap25, and the newly identified potential genes, Tmem65, Grm5, Olfm1, Timp3. Finally, we analyzed the changes of cell communication signaling pathways in neurons before and after synapse formation, and identified several important signaling pathways, including NRXN, NCAM, BMP, NEGR, and so on. Collectively, our work provided a holistic view of the molecular dynamics of the hippocampal synapse formation.

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