α-Synuclein A53T Mice Present with Progressive Motor Decline - August, 2014

Aggregation of α-Synuclein (α-Syn) protein in the brain plays a central role in Parkinson’s disease (PD). The α-Syn over-expressing mouse is therefore a suitable model for studying α-Syn production, sequestration and deposition, and the possible influences of drugs on these parameters. Point mutations in α-Syn (e.g. A53T, A30P, E46K) have been identified in rare forms of familial PD and are reported to accelerate its oligomerization and aggregation. In subjects affected by the α-Syn A53T mutation, the age of onset is much earlier than for sporadic PD. The development of new PD drugs halting the production of α-Syn aggregates and the resultant neurodegeneration is thus the main focus in PD research. To be able to test these new drugs, appropriate animal models are needed.

In this poster, we present how the A53T α-Syn transgenic mouse model imitates critical clinical features of PD, and therefore represents a valuable tool for both basic research related to PD as well as for efficacy tests of new, investigational compounds for the treatment of PD.

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