-synuclein and cytosolic dopamine: Stabilizing a bad situation
David Sulzer
Departments of Neurology and Psychiatry, Columbia University and Department of Neuroscience, New York State Psychiatric Institute New York, New York, USA
ds43@columbia.edu
The intriguing finding that -synuclein—a protein recently found to be mutated in some familial cases of Parkinson disease—and cytosolic dopamine interact to form adducts that stabilize a presumably toxic intermediate of fibril formation provides clues into the mechanism of neurodegeneration.
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-synuclein and cytosolic dopamine: Stabilizing a bad situation
-synuclein—a protein recently found to be mutated in some familial cases of Parkinson disease—and cytosolic dopamine interact to form adducts that stabilize a presumably toxic intermediate of fibril formation provides clues into the mechanism of neurodegeneration.
-synuclein in Parkinson's disease: insights from animal models
