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The expression level of transgenic alpha-synuclein correlates with the severity of Parkinsonian phenotypes in mice.

Wednesday, November 06, 2013 — Poster Session I

4:00 p.m. – 6:00 p.m.

FAES Academic Center (Upper-Level Terrace)




  • C Sgobio
  • J Yu
  • G Liu
  • Y Mateo
  • DM Lovinger
  • H Cai


Alpha-synuclein, the major component of Lewy bodies, has been associated with Parkinson’s disease (PD) and other neurodegenerative disorders. The A53T mutation of alpha-synuclein causes an early onset autosomal dominant form of familiar PD. Despite intensive studies over the past decades, the physiological function alpha-synuclein and its role in the pathogenesis of PD remains elusive. We characterized a novel conditional alpha-synuclein A53T mouse model using the tetracycline gene regulation system, which allowed us to selectively express alpha-synuclein in midbrain dopaminergic neurons. The nigrostriatal dopaminergic pathway targets the dorso-lateral striatum, while the and mesolimbic dopaminergic system targets the ventral-medial stiratum. In particular, we focused on the characterization of the functionality of dopaminergic terminals in striatum in the presence of the PD-related A53T mutation, as well as the behavioral phenotype in consequence of different degree on a-syn expression.

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