October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
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) |
NIA |
NEURO-33 |
Authors
- C Sgobio
- J Yu
- G Liu
- Y Mateo
- DM Lovinger
- H Cai
Abstract
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.
