A53T-ë±-synuclein overexpression mouse model signaling and striatal synaptic plasticity

ABSTRACT: Parkinson’s disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression, or the A53T mutation, of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. Here, we used two mouse lines overexpressing human A53T-SNCA around ages 6 and 18 months and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. High pressure liquid chromatography analysis of striatal neurotransmitter content demonstrated that dopamine (DA) levels correlated directly with the level of expression of SNCA, an observation also observed in SNCA deficient mice. In the striatum of aged A53TSNCA overexpres

ORGANISM(S): Mus musculus

SUBMITTER: Suzana Gispert 

PROVIDER: E-GEOD-20547 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress