<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>119(3)</volume><submitter>Kurz A</submitter><pubmed_abstract>Parkinson's disease (PD) is a neurodegenerative disorder frequent at old age characterized by atrophy of the nigrostriatal projection. Overexpression and A53T-mutation of the presynaptic, vesicle-associated chaperone alpha-synuclein are known to cause early-onset autosomal dominant PD. We previously generated mice with transgenic overexpression of human A53T-alpha-synuclein (A53T-SNCA) in dopaminergic substantia nigra neurons as a model of early PD. To elucidate the early and late effects of A53T-alpha-synuclein on the proteome of dopaminergic nerve terminals in the striatum, we now investigated expression profiles of young and old mice using two-dimensional fluorescence difference in gel electrophoresis (2D-DIGE) and mass spectrometry. In total, 15 proteins were upregulated and 2 downregu</pubmed_abstract><journal>Journal of neural transmission (Vienna, Austria : 1996)</journal><pagination>297-312</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3282907</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A53T-alpha-synuclein-overexpression in the mouse nigrostriatal pathway leads to early increase of 14-3-3 epsilon and late increase of GFAP.</pubmed_title><pmcid>PMC3282907</pmcid><pubmed_authors>Schmidt O</pubmed_authors><pubmed_authors>Kurz A</pubmed_authors><pubmed_authors>May C</pubmed_authors><pubmed_authors>Meyer HE</pubmed_authors><pubmed_authors>Marcus K</pubmed_authors><pubmed_authors>Muller T</pubmed_authors><pubmed_authors>Auburger G</pubmed_authors><pubmed_authors>Gispert S</pubmed_authors><pubmed_authors>Stephan C</pubmed_authors></additional><is_claimable>false</is_claimable><name>A53T-alpha-synuclein-overexpression in the mouse nigrostriatal pathway leads to early increase of 14-3-3 epsilon and late increase of GFAP.</name><description>Parkinson's disease (PD) is a neurodegenerative disorder frequent at old age characterized by atrophy of the nigrostriatal projection. Overexpression and A53T-mutation of the presynaptic, vesicle-associated chaperone alpha-synuclein are known to cause early-onset autosomal dominant PD. We previously generated mice with transgenic overexpression of human A53T-alpha-synuclein (A53T-SNCA) in dopaminergic substantia nigra neurons as a model of early PD. To elucidate the early and late effects of A53T-alpha-synuclein on the proteome of dopaminergic nerve terminals in the striatum, we now investigated expression profiles of young and old mice using two-dimensional fluorescence difference in gel electrophoresis (2D-DIGE) and mass spectrometry. In total, 15 proteins were upregulated and 2 downregu</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Mar</publication><modification>2026-04-08T00:57:46.323Z</modification><creation>2026-04-07T20:00:28.447Z</creation></dates><accession>S-EPMC3282907</accession><cross_references><pubmed>21960009</pubmed><doi>10.1007/s00702-011-0717-3</doi></cross_references></HashMap>