EC and PVC from 14-15 month-old APOE3/3, APOE3/4 and APOE4/4 mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus Musculus
TISSUE(S): Brain
DISEASE(S): Alzheimers Disease
PROVIDER: ST001819 | MetabolomicsWorkbench |
REPOSITORIES: MetabolomicsWorkbench
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| mwtab | Other |
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Project description:Parkinson's Disease (PD) is primarily caused by aggregates of alpha synuclein (SNCA) in dopaminergic neurons of the substantia nigra, but PD is a systemic disease and may lead to PD-associated dementia complex. PD-associated encephalopathy is a late manifestation in PD patients at risk for example owing to mutations of the lysosomal enzyme glucocerebrosidase. Defects of lysosomal waste removal and aggregation of mutant alpha synuclein (SNCA) impacts of the proteome. Here, we studied the proteome of the prefrontal cortex in Pink1-/-SNCA A53T double mutant mice in comparison with their wildtype controls. Pink1-/-SNCA A53T mice carry a loss of function knock-in mutation of PTEN induced kinase (Pink1), plus the human A53T mutation of alpha synuclein (SNCA-A53T) [1, 2]. Homozygous Pink1-/-SNCA A53T double mutant mice were generated by crossing Pink1-/- mice (background: 129/SvEv) with A53T-SNCA-overexpressing PrPmtA mice (background: FVB/N) and then, interbreeding the littermates. Wildtype (WT) control mice are hybrids from a crossbreeding of 129/SvEv and FVB/N mice, which were descended from littermates of the respective single mutant animals. Pink1-/-SNCA A53T mice develop spontaneous motor symptoms at advanced ages, with a progressive incidence above 15 months of age. The phenotype of Pink1-/-SNCA A53T and wildtype control mice was observed during aging. Mice were euthanized at an age of 1-1.5 years (matched with the controls). The cortices were rapidly removed and frozen in liquid nitrogen and processed for label free proteomic analyses.
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