Parkinson’s disease (PD) is a complex disorder caused by a combination of genetic and environmental factors. Recent progress utilising modern genetic technologies has unveiled the increasing contribution of genetics in the pathogenesis of PD, however, there is still a significant proportion of the genetic component to be identified. The majority of genetic studies focus on single nucleotide variants and we propose that part of this ‘missing heritability’ is due to other types of genetic variation, such as retrotransposons. SINE-VNTR-Alus (SVAs) are a hominid specific composite retrotransposon consisting of a CCCTCT repeat, an Alu-like domain, a GC-rich variable number tandem repeat (VNTR), a SINE region and a poly A-tail. There are nearly 3000 SVAs in the reference human genome and a small subset are polymorphic for their presence/absence. SVAs can affect gene expression, mRNA splicing and have been identified as the cause of 12 genetic diseases including X-linked dystonia parkinsonism. The aim of our study was to characterise polymorphic reference SVAs in whole genome sequencing data from the Parkinson’s Progression Markers Initiative (PPMI), a longitudinal PD cohort with extensive clinical and phenotypic data, to address their potential role in the predisposition to and progression of PD. We identified 83 polymorphic reference SVAs in 179 controls and 371 PD cases and using logistic regression did not identify SVAs associated with disease risk. However, analysis of longitudinal data identified 14 SVAs associated with clinical features and progression markers of PD, including a SVA in the intron of the CASP8 gene whose presence was significantly associated with a lower Movement Disorder Society – Unified Parkinson’s Disease Rating Scale total score (FDR corrected p=0.02) after 36 months follow up. This preliminary study has highlighted the potential role of these elements PD progression and further work is required to understand the functional impact of their insertion.