The neuronal protein alpha‐synuclein (α‐Syn) is crucially involved in Parkinson's disease pathophysiology. Intriguingly, torsinA (TA), the protein causative of DYT1 dystonia, has been found to accumulate in Lewy bodies and… Click to show full abstract
The neuronal protein alpha‐synuclein (α‐Syn) is crucially involved in Parkinson's disease pathophysiology. Intriguingly, torsinA (TA), the protein causative of DYT1 dystonia, has been found to accumulate in Lewy bodies and to interact with α‐Syn. Both proteins act as molecular chaperones and control synaptic machinery. Despite such evidence, the role of α‐Syn in dystonia has never been investigated.
               
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