Thwarting dyskinesia by targeting mTORC1

In a mouse model of Parkinson's disease, new evidence shows that L-DOPA, which is used to treat the symptoms of the disease but also causes dyskinesia, results in a persistent activation of the protein kinase mTOR (mammalian target of rapamycin) in a subset of striatal medium spiny neurons. Moreover, blockade of a specific type of mTOR signaling (mTORC1) prevents the development of dyskinesia, but not the antiakinetic benefits produced by L-DOPA. Thus, mTORC1 may be a viable therapeutic target for dyskinesia caused by L-DOPA treatment in patients with Parkinson's disease.