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Monoclonal antibody Prasinezumab slows progression of Parkinson's disease
Last reviewed: 02.07.2025
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In a recent study published in the journal Nature Medicine, a large international team of researchers conducted an exploratory analysis to assess whether the monoclonal antibody prasinezumab, which has previously been found to be effective in slowing the progression of motor features of Parkinson's disease, shows benefit in subgroups of Parkinson's disease patients with more rapid progression of motor degeneration.
One of the hallmarks of Parkinson's disease is the aggregation of α-synuclein, which is thought to spread between neurons and contribute to the pathogenesis of Parkinson's disease. One of the first therapeutic options to target aggregated α-synuclein was the monoclonal antibody prasinezumab, which was investigated in a phase 2 clinical trial in patients with early-stage Parkinson's disease as part of the PASADENA study.
The primary efficacy outcome measure in the Phase 2 PASADENA trials was the Movement Disorder Society-Unified Parkinson's Disease Rating Scale, or MDS-UPDRS.
In this study, the team examined the effect of prasinezumab on slowing the progression of motor degeneration in subgroups of Parkinson’s patients whose disease progressed rapidly. Given that MDS-UPDRS subscores may not show short-term treatment-related changes, monitoring subgroups with rapidly progressing Parkinson’s disease may help improve the signal-to-noise ratio and identify potential effects of the monoclonal antibody.
The PASADENA study included three treatments – placebo, prasinezumab 1500 mg and prasinezumab 4500 mg. Patients were randomly assigned to the three groups after stratification by age (over or under 60 years), gender and use of monoamine oxidase B inhibitors. Patients using other symptomatic Parkinson’s disease medications, such as dopamine agonists or levodopa at baseline, were excluded. In cases where use of these medications was considered necessary, MDS-UPDRS scores were calculated before treatment.
The results showed that prasinezumab is more effective in slowing the progression of motor signs in patients with Parkinson's disease whose disease is progressing rapidly. Subpopulation analysis showed that patients with a diffuse malignant phenotype or those who used monoamine oxidase B inhibitors at baseline, an indicator of rapid disease progression, showed a slower worsening of motor degeneration compared with patients with phenotypes not indicative of rapid disease progression.
MDS-UPDRS Part III, which measures physician-reported motor signs, showed slower worsening or increasing degeneration in patients treated with prasinezumab compared with those receiving placebo. MDS-UPDRS Parts I and II measure patient-reported motor and non-motor signs, respectively.
Overall, the results suggest that the monoclonal antibody prasinezumab has the potential to slow the progression of motor degeneration in patients with rapidly progressive Parkinson's disease. In addition, longer follow-up periods are needed to assess the impact of prasinezumab treatment in patients with slowly progressive disease. Furthermore, additional randomized clinical trials are needed to further confirm these results.