LAUSR

Parkinson disease (PD), similar to other neurodegenerative conditions, is characterized by relentless clinical progression with gradual worsening of both motor and nonmotor features. Potential neuroprotective therapies focusing on aspects of neurodegeneration in PD such as impaired mitochondrial function with abnormalities of oxidative phosphorylation, increased oxidative stress, and suppressed neuroinflammation, have failed to alter the clinical course of PD.1,2 New insights into PD pathophysiology have identified potential molecular targets, including accumulation and potential prion-like spreading of aggregates containing misfolded α-synuclein protein.3 These therapies are only approaching clinical testing, and their true therapeutic potential remains unknown. Even if successful, they are many years away from clinical availability. Thus, at present, we do not have any proven pharmacologic options to modify the progressive decline of patients with PD.