JH Kordower

Co- and multipathologies need serious consideration for understanding Parkinson's disease pathogenesis and designing novel experimental therapeutic strategies

Parkinson ’ s disease (PD) is pathologically de fi ned by the presence of aggregated α -synuclein in the form of Lewy bodies and Lewy neurites. 1 – 4 Considerable interest has focused on anti-α -synuclein immunotherapy as a potential disease-modifying strategy for PD, but initial phase 2a clinical trials examining this approach did not meet their primary endpoint. Most recently, the phase 2b PADOVA trial of prasinezumab, published in The Lancet Neurology , also did not meet its primary endpoint, although a non-signi fi cant delay in motor progression and prespeci fi ed exploratory fi ndings suggested potential clinical activity. 5 – 7