Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease

ABSTRACT: Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease

PROVIDER: PRJNA1062854 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27475038_1.fastq.gz	Fastqsanger.gz
	SRR27475038_2.fastq.gz	Fastqsanger.gz
	SRR27475039_1.fastq.gz	Fastqsanger.gz
	SRR27475039_2.fastq.gz	Fastqsanger.gz
	SRR27475040_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 30

Similar Datasets

Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [sham]

Project description:Parkinson’s disease (PD) is an age-related neurodegenerative disorder characterized by the degeneration of the nigrostriatal dopaminergic neurons, and by intraneuronal accumulation of aggregated α-synuclein (aSyn). Environmental factors contribute significantly to neurodegeneration in patients, and non-pharmacological interventions are increasingly explored. Among these, caloric restriction and time-restricted feeding have demonstrated beneficial effects in animal models of neurodegenerative diseases. The ketone body β-hydroxybutyrate (BHB) has been suggested to mediate some of these effects. In this study, we tested the therapeutic potential of intermittent fasting (IF, every other day feeding) in an aSyn-based mouse model of PD. IF was initiated four weeks after induction of aSyn pathology. Four weeks of IF mitigated the aSyn-induced degeneration of dopaminergic neurons and axon terminals. IF also reduced aSyn pathology as reported by staining for phosphorylated aSyn and Triton X-100 solubility. IF mitigated the aSyn-induced motor phenotype, the decrease in striatal dopamine and the decrease in synaptic markers. In transcriptomic analysis, we observed a robust modulation of genes involved in inflammation and microglia activation even with just brief IF treatment and without synuclein transduction. In primary mouse neurons, starvation and treatment with BHB were sufficient to induce autophagy and reduced αSyn pathology. Taken together, IF might constitute a plausible neuroprotective strategy for patients with Parkinson’s diseases. BHB-induced autophagy and altered neuroinflammation are pathways that potentially contribute to the protective effect.

2025-01-03 | GSE252873 | GEO

Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [asyn]

2025-01-03 | GSE252872 | GEO

Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [asyn]

Project description:Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [asyn]

| PRJNA1062858 | ENA

Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [sham]

Project description:Intermittent fasting reduces alpha-synuclein pathology and functional decline in a mouse model of Parkinson’s disease [sham]

| PRJNA1062857 | ENA

Transcriptome analysis of mouse heart under different intermittent fasting conditions

Project description:Various intermittent fasting regimes are popularly being practiced but the scientific understanding for the mechanisms of intermittent fasting remains unclear. Observing the overall transcriptomic changes in specific organs, including heart, may contribute substantially in understanding the diverse effects of intermittent fasting. Our current study further investigate the differential transcriptomic changes in the heart among the different regimes of intermittent fasting as well.

2023-09-27 | GSE133290 | GEO

Intermittent fasting alters the spatiotemporal atlas of transcriptomes

Project description:Transcription factors may orchestrate the health benefits of intermittent fasting through directing the expression of genome. Here, we find intermittent fasting can spin the spatiotemporal profile of transcription factors, and provide an atlas of transcription factors in biological space, time and feeding regimen.

2022-10-27 | GSE154797 | GEO

Transcriptome analysis reveals intermittent fasting-induced genetic changes in ischemic stroke

Project description:Intermittent fasting is previously reported to exhibit neuroprotection against experimental ischemic stroke. However, the detailed understanding of protection mechanisms are lacking. By observing the overall transcriptomic changes in each timepoint of ischemic stroke would benefit the understanding of underlying active pathways and mechanisms. Here, we conduct experimental MCAO ischemic stroke on mice exposed to different daily intermittent fasting method to compare not only among the ischemic stroke timepoints but also the efficacy of different intermittent fasting interventions. Our current study presented the transcriptomic changes for the first time in specific timepoints of ischemic stroke as well as under the condition of intermittent fasting. A number of neuroprotective mechanisms-related genes were significantly affected by intermittent fasting conditions in differential manners.

2018-07-11 | GSE116878 | GEO

Intermittent fasting triggers interorgan communication to suppress hair follicle regeneration

Project description:Intermittent fasting has gained increasing popularity globally for its potential benefits for improving health and managing weight, but how it impacts the homeostasis and regeneration of peripheral tissues remains elusive. Here we report that in mice, commonly used intermittent fasting regimens negatively affect hair regeneration by selectively inducing apoptosis in activated hair follicle stem cells (HFSCs). Through manipulating animals' daily feeding schedules and caloric intake, we have found that the impaired hair regeneration is primarily caused by the extended fasting periods within these regimens, rather than a reduction in total caloric intake or alterations in circadian rhythm. As the fasting period lengthens, the severity of the defects worsens. Mechanistically, extended periods of fasting activate the hypothalamic-pituitary-adrenal axis, prompting the release of lipolytic hormones from the adrenal glands into circulation. This triggers rapid lipolysis in dermal adipocytes, elevating levels of free fatty acids within the skin. Consequently, fatty acid oxidation is activated in HFSCs, causing increased cellular oxidative stress and apoptosis. Surgical removal of adrenal glands, genetic inhibition of fatty acid oxidation in HFSCs, or enhancement of HFSCs’ antioxidant capability genetically or pharmaceutically prevents fasting-induced stem cell death. Our study reveals a detrimental effect of intermittent fasting on somatic stem cells and peripheral tissue regeneration, and identifies a close crosstalk between an ancient neuroendocrine mechanism and a critical niche component that functions as a “brake” to halt tissue regeneration when the supply of nutrients becomes unstable.

2024-11-07 | GSE246952 | GEO

Phenotypic manifestation of alpha-synuclein strains from Parkinson’s disease and multiple system atrophy in human dopaminergic neruons

Project description:Although α-synucleinis implicated in the pathogenesis of Parkinson’s disease and related disorders, it remains unclear whether specific conformations or levels of α-synuclein assemblies are toxic and how they cause progressive loss of human dopaminergic neurons. To address this issue, we used iPSC-derived dopaminergic neurons with a-synuclein triplication or controls where endogenous α-synuclein was imprinted into synthetic or disease-relevant conformations. We used α-synuclein fibrils generated de novo or amplified from homogenates of brains affected with Parkinson’s disease (n=3) .We found that a 2.5-fold increase in α-synuclein levels in α-synuclein gene triplication neurons promoted seeded aggregation in a dose and time-dependent fashion, which was associated with a further increase in α-synuclein gene expression.Transcriptomic analysis and isogenic correction of α-synuclein triplication revealed that intraneuronal α-synuclein levels solely and sufficiently explained vulnerability to cell death.

2020-09-02 | GSE149632 | GEO

Phenotypic manifestation of alpha-synuclein strains derived from Parkinson’s disease and multiple system atrophy in human dopaminergic neurons

Project description:Althougha-synuclein is implicated in the pathogenesis of Parkinson’s disease and related disorders, it remains unclear whether specific conformations or levels ofa-synuclein assemblies are toxic and how they cause progressive loss of human dopaminergic neurons. To address this issue, we used iPSC-derived dopaminergic neurons with a-synuclein triplication or controls where endogenous a-synuclein was imprinted into synthetic or disease-relevant conformations. We used a-synuclein fibrils generated de novo or amplified from homogenates of brains affected with Parkinson’s disease (n=3) or multiple system atrophy (n=5). We found that a 2.5-fold increase in a-synuclein levels in a-synuclein gene triplication neurons promoted seeded aggregation in a dose and time-dependent fashion, which was associated with a further increase in a-synuclein gene expression. Progressive neuronal loss was observed only in a-synuclein triplication neurons seeded with brain-amplified fibrils. Transcriptomic analysis and isogenic correction of a-synuclein triplication revealed that intraneuronalalpha-synuclein levels solely and sufficiently explained vulnerability to neuronal death

2021-04-13 | GSE171999 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data