Ontology highlight
ABSTRACT:
PROVIDER: PRJNA520742 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8528151.fastq.gz | Fastqsanger.gz | |||
| SRR8528151_1.fastq.gz | Fastqsanger.gz | |||
| SRR8528151_2.fastq.gz | Fastqsanger.gz | |||
| SRR8528147.fastq.gz | Fastqsanger.gz | |||
| SRR8528147_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:People with neurodegenerative disorders have diverse clinical syndromes, genetic heterogeneity, and distinct brain pathological changes, but studies report overlap between these features. DNA methylation (DNAm) is a widely studied chemical modification to DNA, and increasing evidence suggests that DNAm alterations play an important role in neurodegenerative disorders. In this study we aimed to identify shared blood DNAm differences between 471-1,522 controls and people with Alzheimer’s disease (N = 161), amyotrophic lateral sclerosis (N = 3,032) and Parkinson’s disease (N = 1,132). We used a mixed-linear model method (MOMENT) that has been shown to account for the effect of (un)known confounders, to test for association of each DNAm site with each disorder. A fixed-effects meta-analysis of Alzheimer’s disease, amyotrophic lateral sclerosis, and Parkinson’s disease results identified 12 differentially methylated positions passing a genome-wide significant threshold. Predicted immune cell-type proportions were disrupted across all neurodegenerative disorders, as well as schizophrenia and rheumatoid arthritis. Protein inflammatory markers were correlated with profile sum-scores derived from disease-associated immune cell-type proportions in a healthy ageing cohort. In contrast, they were not correlated with MOMENT DNAm-derived profile sum-scores, calculated using effect sizes of the 12 differentially methylated positions as weights. We have identified shared differentially methylated positions in whole blood between neurodegenerative disorders that point to shared pathogenic mechanisms. These shared differentially methylated positions may reflect causes or consequences of disease, but they are unlikely to reflect cell-type proportion differences.
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Project description:WFS1 pull-down in HEK293 cells transfected with WFS1 expression plasmid. Precipitated proteins were separates into 13 fractions by SDS-PAGE, digested with trypsin and analyzed by LC-MS/MS. Samples P1-13 = pull-down with anti-WFS rabbit polyclonal (Cell Signaling Technologies #8749S), samples N14-26 = negative control (rabbit IgG).
Mitochondrial dysfunction involving mitochondria-associated ER membrane (MAM) dysregulation is implicated in the pathogenesis of late-onset neurodegenerative
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