Ontology highlight
ABSTRACT: Background
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.Objective
We explored whether α-Syn and N-ethylmaleimide sensitive fusion attachment protein receptor proteins (SNAREs), that are known to be modulated by α-Syn, may be involved in DYT1 dystonia synaptic dysfunction.Methods
We used electrophysiological and biochemical techniques to study synaptic alterations in the dorsal striatum of the Tor1a+ /
SUBMITTER: Ponterio G
PROVIDER: S-EPMC9323501 | biostudies-literature | 2022 May
REPOSITORIES: biostudies-literature