PerspectiveNeuroscience

Thwarting Dyskinesia by Targeting mTORC1

Science Signaling  21 Jul 2009:
Vol. 2, Issue 80, pp. pe42
DOI: 10.1126/scisignal.280pe42

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Abstract

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.

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