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Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [ST]

ABSTRACT: Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [ST]

PROVIDER: PRJNA1195002 | ENA |

REPOSITORIES: ENA

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Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

Project description:Evidence suggests that Lewy body pathology in Parkinson's disease (PD) may originate in the gut, with intestinal inflammation serving as an early mediator via the gut-brain axis. Mutations in leucine-rich repeat kinase 2 (LRRK2) are a common genetic risk factor for both PD and inflammatory bowel disease. We proposed that modulating the gut microenvironment could assist in mitigating PD progression, particularly in individuals with LRRK2 mutations. Our study indicates that germ-free condition could only partially alleviate PD process in LRRK2 G2019S mice. Mono-inoculation of PG in germ-free LRRK2 G2019S mice mitigated age-dependent motor dysfunction. In the brain, the colonic P. goldsteinii treatment reduces neuronal a-synuclein expression, ease neuroinflammation, and mitigates dopaminergic degeneration. In the gut, the PG administration suppressed the toll-like receptor 4 signaling, facilitated the differentiation of intestinal dendritic cells and macrophages, and increased the abundance of anti-inflammatory T cells. Our findings demonstrated that colonization by P. goldsteinii alleviates the progression of PD by exerting multifaceted effects in maintaining intestinal homeostasis.

2025-06-27 | GSE284454 | GEO

Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [ST]

Project description:Our study confirms that gut microbiota is essential for motor dysfunction and neuropathology in LRRK2 G2019S mice. Monoculturing Parabacteroides goldsteinii mitigates age-related motor dysfunction, alpha-synuclein expression, neuroinflammation, and dopaminergic degeneration. Its effects on the gut microenvironment include suppressing the toll-like receptor 4 signaling pathway, facilitating the differentiation of intestinal dendritic cells and macrophages, and promoting anti-inflammatory intraepithelial CD4+ CD8αα+ T cells. It also upregulates tissue repair and immune differentiation pathways, enhances intestinal epithelial junction and mitochondrial function genes, and reduces colonic alpha-synuclein levels.

2025-08-01 | GSE283669 | GEO

Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [RNA-seq]

2025-08-01 | GSE283666 | GEO

Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [RNA-seq]

Project description:Gut Commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism through reducing neuroinflammation and multifaceted effects on gut homeostasis [RNA-seq]

| PRJNA1195008 | ENA

Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

Project description:Gut commensal Parabacteroides goldsteinii mitigates LRRK2 Parkinsonism by reducing neuroinflammation and enhancing gut homeostasis

| PRJNA1199076 | ENA

Parabacteroides goldsteinii

Project description:Parabacteroides goldsteinii overview

| PRJNA64965 | ENA

Gene expression data from LRRK2-WT and LRRK2-G2019S astrocytes

Project description:LRRK2-G2019S (LRRK2-GS), a pathogenic mutation in the PD-associated gene LRRK2, promote ER stress-induced cell death by reducing transcriptional activity of X-box-binding protein 1 (XBP1), a key transcription factor of the UPR. We used microarrays to detail the programme of gene expression and identified distinct classes of up-regulated or down-regulated genes during ER stress.

2019-10-31 | GSE139579 | GEO

Ribosome profiling experiments of LRRK2 mouse models

Project description:G2019S mutaion of LRRK2 is known to increase mRNA translation. We perform ribosome profiling to study defective translation in mammalian LRRK2 models. We used G2019S LRRK2 transgenic mice, G2019S/D1994A LRRK2 transgenic mice, LRRK2 knockout mice.

2021-02-27 | GSE167704 | GEO

Gene and microRNA transcriptome analysis of Parkinson's related LRRK2 mouse models

Project description:Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent cause of familial and sporadic ParkinsonM-bM-^@M-^Ys disease (PD). Here, we investigated in parallel gene and microRNA transcriptome profiles of three different LRRK2 mouse models. Striatal tissue was isolated from adult LRRK2 knockout mice, as well as mice expressinghuman LRRK2 wildtype (hLRRK2-WT) or PD-associated R1441G mutation (hLRRK2-R1441G). We used microarraya to measure gene and microRNA expression levels in various LRRK2 mouse models. LRRK2 wildtype and knockout mice were bred on a C57BL/6 background. LRRK2 non-transgenic and hLRRK2 transgenic mice were bred on a FVB/N background.

2013-11-22 | E-GEOD-52584 | biostudies-arrayexpress

Modelling G2019S-LRRK2 sporadic Parkinson’s disease in 3D midbrain organoids

Project description:Recent advances in generating 3 dimensional (3D) organoid systems from stem cells offer new possibilities for disease modeling. In this study, we generate isogenic 3D midbrain organoids with or without a Parkinson’s disease-associated LRRK2 G2019S mutation. LRRK2-G2019S midbrain organoids derived from LRRK2 targeted human iPSCs in vitro have LRRK2-associated sporadic Parkinson's disease phenotypes. Midbrain-like 3D organoids expressing LRRK2-G2019S showed dynamic changes in globle gene expression.

2019-02-02 | GSE125234 | GEO

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