Aggregated α-synuclein is a feature of Parkinson disease (PD). Indeed, some cases of familial PD are caused by point mutations in or duplication of the α-synuclein gene (SNCA). Nevertheless, how α-synuclein contributes to disease pathophysiology and its physiological roles remain to be fully understood. Now, Hallacli et al. show that α-synuclein can interact with protein components of processing bodies (P-bodies) — membraneless organelles involved in mRNA metabolism — and that such interactions can affect mRNA stability and be relevant to disease.

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