Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genes critical for development and differentiation of dopaminergic neurons are downregulated in Parkinson’s disease

ABSTRACT: We performed transcriptome analysis using RNA sequencing on substantia nigra pars compacta (SNpc) from mice after acute and chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment and Parkinson’s disease (PD) patients.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE206308 | GEO | 2022/06/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Neuroprotective effect of a medium-chain triglyceride ketogenic diet on MPTP-induced Parkinson’s disease mice: A combination of transcriptomics and metabolomics in the substantia nigra and fecal microbiome

Project description:To explore effect of medium-chain triglyceride KD (MCT-KD) in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model, we profiled substantia nigra pars compacta tissues from control group, MPTP group and MPTP + KD mice by RNA sequencing (RNA-seq).

2023-08-01 | GSE232039 | GEO

Whole Transcriptome Analysis of Substantia Nigra in Mice with MPTP-Induced Parkinsonism Bearing Defective Glucocerebrosidase Activity

Project description:We characterized the transcriptomic profiles of cells from the substantia nigra (SN) of mice with co-injection with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and selective inhibitor of GCase activity (conduritol-β-epoxide, (CBE)) to mimic PD bearing GCase dysfunction (MPTP+CBE), mice treated with MPTP, mice treated with CBE and control mice treated with injec-tion of sodium chloride (NaCl) (vehicle).

2023-08-31 | E-MTAB-13244 | biostudies-arrayexpress

Methylphenidate exposure induces dopamine neuron loss and activation of microglia in the basal ganglia of mice

Project description:Background: Methylphenidate (MPH) a psychostimulant prescribed to manage ADHD symptoms, has been increasingly prescribed to children not meeting the strict criteria for ADHD. It has also been misused as a “cognitive enhancer” and as an alternative to other psychostimulants. Here, we investigate whether chronic or acute administration of methylphenidate in mice at either 1mg/kg or 10mg/kg dosing, affects cell number and gene expression in the basal ganglion. Methodology/Principal findings: Through the use of stereological counting methods, we observed a significant reduction (~20%) in dopamine neuron numbers in the substantia nigra pars compacta (SNpc) following chronic administration of 10mg/kg MPH. This dosage of MPH also induced a significant increase in the number of morphologically-activated SNpc microglia. Additionally, exposure to either 1mg/kg or 10 mg/kg MPH increased the sensitivity of SNpc dopamine neurons to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced oxidative stress. Unbiased gene screening employing Affymetrix GeneChip® HT MG-430 PM revealed changes in 115 and 54 genes in the substantia nigra (SN) of mice exposed to 1mg/kg and 10mg/kg MPH doses, respectively. Decreases in the mRNA levels of gdnf, dat1, vmat2 and th in the substantia nigra (SN) was observed with both acute and chronic dosing of 10mg/kg MPH. We also found an increase in mRNA levels of the pro-inflammatory genes il-6 and tnf-α in the striatum; although these were seen only at an acute dose of 10mg/kg and not following chronic dosing. Conclusion: Collectively our results suggest that chronic MPH usage in mice, especially at prolonged higher doses, has long-term neurodegenerative consequences. drug treatment: 3 control, 3 low dose treatment, 3 high dose treatment

2012-08-13 | E-GEOD-33619 | biostudies-arrayexpress

Microarray Studies in the Laser Capture Microdissected SNc after a Single Administration of MPTP in Common Marmosets

Project description:We have previously detected cyclin D1-initiated and p53-related (PERP; p53 apoptosis-associated target) cell death in a striatal 6-hydroxydopamine (6-OHDA)-treated Parkinsonian mouse model by adaptor-tagged competitive PCR (ATAC-PCR) (Synapse 51, 279-286, 2004). In order to establish the mechanism of dopaminergic cell death in Parkinson’s disease, various Parkinsonian animal models should be studied. Therefore, the time-course alteration of gene expression in the substantia nigra pars compacta was investigated after a single administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in common marmosets. In the MPTP model, gene expression of neither cyclin D1 nor PERP was altered. There were also few common alterations in gene expression between the MPTP and 6-OHDA models. This suggests that the mechanism of cell death may differ between these models, and extensive study in various Parkinsonian models should be performed to elucidate the mechanisms of dopaminergic cell death in Parkinson’s disease. Keywords: time course

2006-06-29 | GSE5176 | GEO

Methylphenidate exposure induces dopamine neuron loss and activation of microglia in the basal ganglia of mice

2012-08-14 | GSE33619 | GEO

Gene expression data from substantia nigral regions of MPTP-intoxicated mouse brain by acupuncture

Project description:Parkinson’s disease (PD) is a representative neurodegenerative disease that is characterized the death of dopamine-generating cells in the substantia nigra (SN). Acupuncture stimulations at GB34 and LR3 resulted in the enhanced survival of dopaminergic neurons in the SN in the parkinsonism animal models. SN is known as an important player in brain function, in particular, movement. Behavioral tests showed that acupuncture stimulations improved the motor dysfunction in a previous study by almost 87.7%. This study investigated the changes of gene expression profiles in the SN regions of the relatively chronic parkinsonism model and demonstrated the genes that may be related to the inhibitory effect of acupuncture on the change in gene expression in the SN induced by an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxication using a whole transcript array. We investigated gene expression profile changes in the substantia nigral region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism models after acupuncture at the acupoints GB34 and LR3

2014-12-27 | GSE48293 | GEO

A primate nigrostriatal atlas of neuronal vulnerability and resilience in a model of Parkinson’s disease

Project description:The degenerative process in Parkinson’s disease (PD) causes a progressive loss of dopaminergic neurons (DaNs) in the nigrostriatal system. Resolving the differences in neuronal susceptibility warrants an amenable PD model that, in comparison to post-mortem human specimens, controls for environmental and genetic differences in PD pathogenesis. At present study, we generated a primate model of PD by carotid artery injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine MPTP and sampled substantia nigra and putamen of macaque for single cell sequencing analysis.

2023-11-19 | E-MTAB-13437 | biostudies-arrayexpress

RNA-SEQ profiling of dopaminergic neurons from the substantia nigra pars compacta and ventral tegmental area regions of the mouse mid-brain

Project description:RNA-SEQ profiling of dopaminergic neurons from the substantia nigra pars compacta and ventral tegmental area regions of the mouse mid-brain Murine midbrain dopaminergic neurons from the SNpc and VTA regions

2015-07-27 | E-GEOD-64452 | biostudies-arrayexpress

Beta-synuclein potentiates synaptic vesicle dopamine uptake and rescues dopaminergic neurons from MPTP-induced death in the absence of other synucleins

Project description:Previous studies demonstrated that dopaminergic neurons in the substantia nigra pars compacta (SNpc) of mice with null mutations for genes encoding a-synuclein and/or y-synuclein are resistant to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. An original straightforward interpretation of these results was that these proteins are directly involved in the mechanism of MPTP-induced degeneration and this view has become commonly accepted. Here we provide evidence that a plausible explanation of this resistance is not the absence of these synucleins per se but their substitution on the membrane of synaptic vesicles by the third member of the family, b-synuclein. Dopaminergic neurons of mice lacking b-synuclein singularly or in combination with the loss of other synucleins, were sensitive to the toxic effect of MPTP. Dopamine uptake by synaptic vesicles isolated from the striatum of triple a/b/y-synuclein deficient mice was significantly reduced, while reintroduction of b-synuclein either in vivo or in vitro reversed this effect. Proteomic analysis of complexes formed on the surface of synuclein-free synaptic vesicles after addition of recombinant b-synuclein identified multiple integral constituents of these vesicles as well as typically cytosolic proteins, including key enzymes involved in dopamine synthesis, tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC). Therefore, b-synuclein plays a scaffolding role for the assembly of molecular complexes that enhance the ability of synaptic vesicles to uptake and sequester dopamine and other structurally similar molecules, including MPP+. Deficiency of b-synuclein therefore results in the accumulation of MPP+ in the cytosol, where it imposes a damaging effect on presynaptic terminals and ultimately the destruction of dopaminergic neurons.

2021-11-29 | PXD027667 | Pride

Age-mediated transcriptomic changes in adult mouse substantia nigra

Project description:Substantia nigra pars compacta (SNpc) is highly sensitive to normal aging and selectively degenerates in Parkinson's disease. Until now, molecular mechanisms behind SNpc aging have not been fully investigated using high throughput techniques. Here, aging-associated early changes in transcriptome of SNpc were investigated comparing late middle-aged (18 months old) to young (2 months old) mice.

2013-05-29 | GSE45043 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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