Breathing new life into an old target: Pulmonary disease drugs for Parkinson's disease therapy

Abstract

Increases in α-synuclein protein expression are suspected to increase the risk of the development of Parkinson's disease (PD). A recent study has demonstrated that β2-adrenergic receptor (β2AR) agonists decrease histone acetylation in the α-synuclein gene and suppress transcription. Coupled with the anti-inflammatory effects that are associated with β2AR activation, this two-pronged attack holds promise for PD treatment and the development of new therapeutic approaches for this disease.