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GPR34 senses demyelination to promote neuroinflammation and cognition impairment in Alzheimer's disease

ABSTRACT: GPR34 senses demyelination to promote neuroinflammation and cognition impairment in Alzheimer's disease

PROVIDER: PRJNA892590 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21986228_1.fastq.gz	Fastqsanger.gz
	SRR21986228_2.fastq.gz	Fastqsanger.gz
	SRR21986229_1.fastq.gz	Fastqsanger.gz
	SRR21986229_2.fastq.gz	Fastqsanger.gz
	SRR21986230_1.fastq.gz	Fastqsanger.gz

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GPR34 senses demyelination to promote neuroinflammation and cognition impairment in Alzheimer's disease

Project description:Sterile neuroinflammation initiated by damage-associated molecular patterns (DAMPs) has been regarded as an important driver in Alzheimer's disease (AD) and can occur prior or independently of the deposition of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles (NFTs). Genetic ablation or pharmacological inhibition of GPR34 reduced microglia activation, Aβ deposition and cognition impairment. Moreover, GPR34 inhibition prevented aging associated neuroinflammation and cognition impairment without the presence of Aβ plaques.

2025-02-05 | GSE216209 | GEO

GPR34 senses myelin debris to promote neuroinflammation and pathology

Project description:Sterile neuroinflammation is a major driver of multiple neurological diseases. Myelin debris, which is released from the damaged myelin sheaths during demyelination, can act as an inflammatory stimulus to promote sterile inflammation and neurological pathologies, but the mechanism is poorly understood. Here, we show that lysophosphatidylserine (LysoPS)-GPR34 axis plays a critical role in microglia-mediated myelin debris sensing and the subsequent neuroinflammation. Myelin debris-induced microglia activation and proinflammatory cytokine expression relied on its lipid component LysoPS. Both myelin debris and LysoPS promoted microglia to produce IL-1and IL-6 via GPR34 and its downstream PI3K-AKT and ERK signaling. In vivo, LysoPS production and GPR34 signaling were found to be essential for neuroinflammation and pathologies in the mouse models of multiple sclerosis and stroke. Importantly, pharmacologic blockade of GPR34 showed potential therapeutic effects on these disease models. Thus, our results identify GPR34 as a key receptor to sense myelin debris and promote neuroinflammation, and suggest it as a potential target for demyelination-associated diseases.

2025-01-30 | GSE195741 | GEO

GPR34 senses demyelination to promote neuroinflammation and pathologies.

Project description: Not available

| S-EPMC11442997 | biostudies-literature

GPR34 senses myelin debris to promote neuroinflammation and pathology

Project description:GPR34 senses myelin debris to promote neuroinflammation and pathology

| PRJNA802043 | ENA

Investigating GPR34 expression regulation using whole transcriptome sequencing of spleens and dendritic cells from wildtype and GPR34 knockout mice

Project description:Naive spleens as well as naive and LPS-treated dendritic cells from wildtype and GPR34-/- mice were sequenced to integrate expression profiles with protein interaction networks and find functional modules that are affected by GPR34 Expression profiles of dendritic cells and whole spleens were generated using Illumina HiSeq 2500/ Illumina HiScan

2016-03-02 | E-GEOD-68155 | biostudies-arrayexpress

Therapeutic reactivation of hippocampal progenitors reverses cognition decline in progressive brain demyelination

Project description:Therapeutic reactivation of hippocampal progenitors reverses cognition decline in progressive brain demyelination

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Therapeutic reactivation of hippocampal progenitors reverses cognition decline in progressive brain demyelination

Project description:Chronic brain demyelination and neurodegeneration are pathological hallmarks of progressive multiple sclerosis (MS) that underlie cognitive impairments. Neural precursor cells (NPCs) that reside in the hippocampus support cognition through adult neurogenesis. However, with MS chronicity, hippocampal neurogenesis declines that results in memory and learning impairments. Currently, the underlying mechanisms that drive NPC senescence in chronic MS are largely unknown. Here, we have linked downregulation of Neuregulin-1beta 1 (Nrg-1β1) to hippocampal neurodegeneration, neurogenic decline and memory impairment in mice with chronic brain demyelination. Nrg-1β1 is a key factor for neural differentiation that we previously reported its downregulation in chronic human MS lesions. Here, extensive in vivo and in vitro characterizations revealed that therapeutic restoration of Nrg-1β1 can reactivate NPCs and foster hippocampal repair by neurogenesis, synapse reassembly and remyelination that reverses memory impairments. Transcriptomics of NPC progenies confirmed upregulation of genes associated with myelination, synaptic resilience, and cellular homeostasis, underscoring the potential of Nrg-1β1 in activating regenerative mechanisms within the chronically demyelinated hippocampus. Moreover, in comparison with Siponimod, a leading disease modifying therapy for secondary progressive MS, Nrg1β1 treatment achieved multifaceted and greater reparative effects. These new findings introduce Nrg1β1 as a disease relevant candidate with promising therapeutic potential for progressive MS.

2026-03-24 | GSE287967 | GEO

Investigating GPR34 expression regulation using whole transcriptome sequencing of spleens and dendritic cells from wildtype and GPR34 knockout mice

2016-03-02 | GSE68155 | GEO

Bulk transcriptome analysis of wildtype, TREM2 knockout, GPR34 knock-out or TREM2/GPR34 double knock-out iPSC-derived human microglia treated either with PBS or myelin.

Project description:Microglia are broadly implicated in modifying disease risk in the central nervous system (CNS). Identifying regulators of microglia state is critical for elucidating their role in disease and identifying novel drug targets. GPR34 is a G-protein coupled receptor expressed in homeostatic microglia where its function is not well understood. Like TREM2, GPR34 detects lipid ligands. Here, we report that GPR34 knockout (KO) maintains lipid homeostasis and rescues dysregulated cholesterol metabolism in TREM2 KO human iPSC-derived microglia (iMG). Loss of GPR34 reduced ERK signaling in iMG, which has been implicated as a signaling pathway dysregulated in AD, with GPR34 agonism shown to promote GPR34 interaction with ERK in a matter consistent with endosomal signaling. In both healthy and amyloid mouse models, Gpr34 KO accelerated microglial state transcriptionally and histologically consistent conversion of homeostatic microglia to a disease-associated microglia (DAM) state. Shifts in microglial state were accompanied by increased expression of multiple metabolic gene sets.

2026-07-21 | GSE293037 | GEO

GPR34 regulation of disease-associated microglial states in mice

Project description:We investigated the role of the microglia-enriched G protein–coupled receptor GPR34 in regulating cell states for microglia and other cell types under physiological and disease conditions using single-cell RNA sequencing (scRNA-seq) and single-nuclei RNA sequencing (snRNA-seq). Microglia isolated from Gpr34 knockout (KO) and wild-type mice, with or without the 5xFAD Alzheimer’s disease background, were profiled to assess transcriptional changes associated with GPR34 loss, as were other cell types in the hippocampus. Our findings indicate that GPR34 plays a critical role in maintaining microglial homeostasis and restraining disease-associated transcriptional responses in vivo.

2026-04-09 | GSE327428 | GEO

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