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Targeting Histone K4 Trimethylation for Treatment of Cognitive and Synaptic Deficits of Mouse Models of Alzheimer's Disease (ChIP-seq)

ABSTRACT: Targeting Histone K4 Trimethylation for Treatment of Cognitive and Synaptic Deficits of Mouse Models of Alzheimer's Disease (ChIP-seq)

PROVIDER: PRJNA746404 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15120462.fastq.gz	Fastqsanger.gz
	SRR15120463.fastq.gz	Fastqsanger.gz
	SRR15120464_1.fastq.gz	Fastqsanger.gz
	SRR15120464_2.fastq.gz	Fastqsanger.gz
	SRR15120465.fastq.gz	Fastqsanger.gz

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Targeting Histone K4 Trimethylation for Treatment of Cognitive and Synaptic Deficits of Mouse Models of Alzheimer's Disease

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Targeting histone K4 trimethylation for treatment of cognitive and synaptic deficits in mouse models of Alzheimer's disease.

Project description:Epigenetic aberration is implicated in aging and neurodegeneration. Using postmortem tissues from patients with Alzheimer's disease (AD) and AD mouse models, we have found that the permissive histone mark H3K4me3 and its catalyzing enzymes are significantly elevated in the prefrontal cortex (PFC). Inhibiting H3K4-specific methyltransferases with the compound WDR5-0103 leads to the substantial recovery of PFC synaptic function and memory-related behaviors in AD mice. Among the up-regulated genes reversed by WDR5-0103 treatment in PFC of AD mice, many have the increased H3K4me3 enrichment at their promoters. One of the identified top-ranking target genes, Sgk1, which encodes serum and glucocorticoid-regulated kinase 1, is also significantly elevated in PFC of patients with AD. Administration of a specific Sgk1 inhibitor reduces hyperphosphorylated tau protein, restores PFC glutamatergic synaptic function, and ameliorates memory deficits in AD mice. These results have found a novel epigenetic mechanism and a potential therapeutic strategy for AD and related neurodegenerative disorders.

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Targeting Histone K4 Trimethylation for Treatment of Cognitive and Synaptic Deficits of Mouse Models of Alzheimer's Disease

Project description:This SuperSeries is composed of the SubSeries listed below.

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Targeting Histone K4 Trimethylation for Treatment of Cognitive and Synaptic Deficits of Mouse Models of Alzheimer's Disease (ChIP-seq)

Project description:We performed chromatin immunoprecipitation sequencing (ChIPseq) to profile genome-wide occupancy of H3K4me3 in PFC from WT mice and P301S Tau mice

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Project description:Epigenetic dysregulation, which leads to the alteration of gene expression in the brain, is suggested as one of the key pathophysiological bases of aging and neurodegeneration. Here we found that, in the late-stage familial Alzheimer’s disease (FAD) mouse model, repressive histone H3 dimethylation at lysine 9 (H3K9Me2) and euchromatic histone methyltransferases, EHMT1 and EHMT2 (H3K9Me2 catalyzer), were significantly elevated in the prefrontal cortex (PFC) region of post-mortem tissues from human patients with Alzheimer's disease. Concomitantly, H3K9Me2 at the promoter region of glutamate receptors was increased in PFC of aged FAD mice, which was linked to the diminished transcription, expression and function of AMPA and NMDA receptors. Treatment of FAD mice with specific EHMT1/2 inhibitors reversed histone hyper-methylation and led to the recovery of glutamate receptor expression and excitatory synaptic function in PFC and hippocampus. Chromatin immunoprecipitation-sequencing (ChIP-seq) data indicated that FAD mice exhibited genome-wide increase of H3K9Me2 enrichment at genes involved in neuronal signaling (including glutamate receptors), which was reversed by EHMT1/2 inhibition. Moreover, the impaired recognition memory, working memory, and spatial memory in aged FAD mice were rescued by the treatment with EHMT1/2 inhibitors. These results suggest that disrupted epigenetic regulation of glutamate receptor transcription underlies the synaptic and cognitive deficits in Alzheimer's disease, and targeting histone methylation enzymes may represent a novel therapeutic strategy for this prevalent neurodegenerative disorder.

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