Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human striatal glia differentially contribute to AD and PD-specific neurodegeneration

ABSTRACT: Alzheimer disease (AD) and Parkinson disease (PD) are the two most common forms of neurodegenerative diseases without effective disease modifying treatments. Despite decades of intensive research, the molecular mechanism of neurodegeneration remains uncertain. We performed the first single-nucleus transcriptome comparison between AD and PD brains.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161045 | GEO | 2022/12/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Human striatal glia differentially contribute to AD and PD-specific neurodegeneration

Project description:Human striatal glia differentially contribute to AD and PD-specific neurodegeneration

| PRJNA675355 | ENA

Proteomics on post-mortem human brain tissue of patients with Alzheimer`s, Parkinson`s and Lewy body dementias.

Project description:We have used HiRIEF (High Resolution Isoelectric Focusing) LC-MS proteomics with isobaric tags (TMT10plex) to compare 32 post-mortem human brains in the prefrontal cortex (Brodmann area 9) of prospectively followed patients with Alzheimer`s disease (AD), Parkinson`s disease with dementia (PDD), dementia with Lewy bodies (DLB) and older adults without dementia.

2017-12-08 | PXD006122 | Pride

Global quantitative analysis of the human brain proteome in Alzheimer’s and Parkinson’s Disease

Project description:Patients with Alzheimer’s disease (AD) and Parkinson disease (PD) often have overlap in brain neuropathology and clinical presentation suggesting that these two diseases share common underlying mechanisms. Currently, the molecular events linking AD and PD are incompletely understood. Utilizing 10-plex Tandem Mass Tag (TMT) assays and MultiNotch MS3 mass spectrometry, we performed an unbiased quantitative proteomic analysis of post-mortem human brain tissues (n=80) from four different groups defined as healthy controls, AD, PD, and co-morbid AD/PD cases across two brain regions (frontal cortex and anterior cingulate gyrus). In total, we identified 11,840 protein groups representing 10,230 gene symbols, which map to ~65% of the protein coding genes in brain. The utility of including two reference standards in each TMT 10-plex assay to assess intra-batch and inter-batch variance is also described. Ultimately, this comprehensive human brain proteomic dataset serves as a valuable resource for various research endeavors including, but not limited to, the identification of protein signatures and neuro-centric signaling pathways that are common or distinct in AD and PD.

2018-02-07 | PXD007160 | Pride

Neuronal deletion of the circadian clock gene Bmal1 induces cell-autonomous dopaminergic neurodegeneration

Project description:Circadian rhythm dysfunction is a hallmark of Parkinson Disease (PD), and diminished expression of the core clock gene Bmal1 has been described in PD patients. BMAL1 is required for core circadian clock function, but also serves non-rhythmic functions. Germline Bmal1 deletion can cause brain oxidative stress and synapse loss in mice, and can exacerbate dopaminergic neurodegeneration in response to MPTP. Here we examined the impact of cell type-specific Bmal1 deletion on dopaminergic neuron viability in vivo. We observed that global, post-natal deletion of Bmal1 caused spontaneous loss of tyrosine hydroxylase-positive (TH+) dopaminergic neurons in the substantia nigra pars compacta (SNpc). This was not due to disruption of behavioral circadian rhythms, and was not induced by astrocyte- or microglia-specific Bmal1 deletion. However, either pan-neuronal or TH neuron-specific Bmal1 deletion caused cell-autonomous loss of TH+ neurons in the SNpc. Finally, global Bmal1 deletion exacerbated TH+ neuron loss following injection of alpha-synclein fibrils. Transcriptomic analysis of neuron-specific Bmal1 KO brain revealed dysregulation of pathways involved in oxidative phosphorylation and Parkinson Disease.

2023-08-18 | GSE241200 | GEO

Dysregulation of microRNAs in neurodegeneration

Project description:This dataset contains small RNA-seq data from six Alzheimer disease, three tangle-predominant dementia and seven control brains.

2014-11-21 | GSE63501 | GEO

Differential activation states of direct pathway striatal output neurons associated with the development of L-DOPA-induced dyskinesia II

Project description:L-DOPA-induced dyskinesia (LID) is a debilitating motor side effect arising from chronic dopamine replacement therapy with L-DOPA for the treatment of Parkinson disease (PD). We found repeated L-DOPA exposure induces unique transcriptional behavior in striatal neurons that is associated with the development of dyskinetic behaviors. These results suggest the development of a long-term neuronal engram underlying the persistence of LID .

2023-12-31 | GSE250362 | GEO

Differential activation states of direct pathway striatal output neurons associated with the development of L-DOPA-induced dyskinesia I

2023-12-31 | GSE250361 | GEO

Transcription profiling of SH-SY5Y cells after treatment with soluble Abeta42_wt, Abeta42_G33A and Abeta40 for different timepoints

Project description:Although amyloid-beta42 (Abeta42) has long been implicated in the pathogenesis of Alzheimer disease (AD), the biological basis of its effects remains uncertain. Intraneuronal Abeta accumulation in brains of patients with AD or Down syndrome, in animal models, and in cultured cells has suggested an early pathophysiological role specific for intracellular Abeta40 and Abeta42. As a consequence of intraneuronal oligomerization, cell death can result from ER stress, endosomal/lysosomal leakage, and mitochondrial dysfunction. A possible nuclear role of intraneuronal Abeta has remained unexplored so far. We here study the role of intranuclear Abeta40 versus Abeta42 and Abeta42_G33A, and an untreated vehicle control in synchronized SH-SY5Y cells. RNA samples for microarray gene expression profiling were collected at t=0, 2, 6, 8 and 12 hours after incubation with Abeta40, Abeta42 and Abeta42_G33A peptides, respectively.'

2014-12-01 | E-MTAB-1841 | biostudies-arrayexpress

GSTM3 single nucleotide polymorphism (rs7483) associated with peripheral BMC expression in Alzheimer disease

Project description:Comparisons between the sample groups (normal elderly control (NEC) and Alzheimer disease (AD)) allowed the identification of genes with disease expression patterns associated with the glutathione S-transferase M3 single nucleotide polymorphism rs7483. Keywords: biological repeat Peripheral blood mononuclear cells (BMC) were obtained from normal elderly control (NEC) and Alzheimer disease (AD) subjects. Targets from biological replicates of NEC (n=18) and AD (n=16) were generated and the expression profiles were determined using the NIA Human MGC cDNA microarray.

2010-06-24 | E-GEOD-4227 | biostudies-arrayexpress

Proteomics on post-mortem human brain tissue of patients with Alzheimer`s, Parkinson`s and Lewy body dementias, Brodmann areas (BA) 9, 24 and 40.

Project description:We have used HiRIEF (High Resolution Isoelectric Focusing) LC-MS proteomics (Branca et al., 2014, PMID: 24240322) with isobaric tags (TMT10plex) to compare 32 post-mortem human brains in the prefrontal cortex (Brodmann areas 24 and 40) of prospectively followed patients with Alzheimer`s disease (AD), Parkinson`s disease with dementia (PDD), dementia with Lewy bodies (DLB) and older adults without dementia. LCMS raw files deposited here refer to samples from BA24 and BA40. For BA09 raw files, refer to the older dataset PXD006122. Proteomics database search files for all three Brodmann areas (BA09, BA24 and BA40) are posted here.

2024-06-10 | PXD047324 | Pride

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