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Z. Gan-Or

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Open access Jul 2026

Genome-wide association studies identify genetic determinants of synucleinopathy biomarkers

Background α-Synucleinopathies are clinically and biologically heterogeneous disorders lacking reliable biomarkers to assist with early diagnosis, disease progression, patient stratification, and therapeutic targeting. Genetic variation is known to impact biomarker levels, influencing their utility and interpretation in research and clinical settings. We aimed to identify common genetic modulators of biomarker levels implicated in α-synucleinopathy pathogenesis. Methods 63 CSF, plasma, and urine biomarkers were analyzed in 581 individuals from the Parkinson’s Progression Markers Initiative (PPMI). GWAS was performed to test for associations with common variants, while regressions and area under the curve (AUC) analysis was used to assess predictive power. Analyses were adjusted for age, sex, disease status, and principal components. PD- and DLB-risk loci associations were separately assessed for each GWAS. Results We confirm strong associations between urine bis(monoacylglycerol)phosphate (BMP) isoforms and the variants LRRK2 p.G2019S and GBA1 p.N370S, while providing support for BMPs use as a LRRK2-PD biomarker. CSF Aβ was significantly associated with an APOE ε4 allele, reinforcing its central role in amyloid regulation. Novel associations were detected between CSF ceramide isoforms the MCF2L2 and GMNN loci, and between CSF tau and the TP63 locus. Multiple PD risk loci, including MAPT, SIPA1L2, MCCC1, and RAB29, were associated with lysosomal lipid biomarkers, highlighting pathway-level convergence. Conclusions The present study reveals established and novel genetic modulators of potential α-synucleinopathy biomarkers, demonstrating that genetic background significantly shapes biomarker levels. These genetic influences should be accounted for when conducting biomarker-based research, clinical trials, or therapeutic development to ensure accurate interpretation and improve their translational relevance.

E. Somerville, Lang Liu, Michael Ta et al. · 0 citations
Open access Aug 2026

Rare-Variant Burden Analysis of Dystonia Genes in Parkinson's Disease.

BACKGROUND Dystonia frequently coexists with Parkinson's disease (PD), yet the extent of genetic overlap remains insufficiently explored. OBJECTIVE The aim was to examine whether rare variants in dystonia-related genes are associated with PD or early-onset PD (EOPD). METHODS We curated 44 dystonia-related genes using the Online Mendelian Inheritance in Man (OMIM) and the Movement Disorder Society report on hereditary dystonia. Whole-genome sequencing data from 5315 PD patients, including 300 EOPD patients, and 36,902 controls across the Accelerating Medicines Partnership-Parkinson's Disease (AMP-PD) and UK Biobank European cohorts were analyzed. Rare-variant burden analysis was performed using the optimized sequence kernel association test (SKAT-O) and MetaSKAT. RESULTS In the analyses of all PD patients, no association survived multiple-testing correction. Conversely, exploratory EOPD analyses identified five significant genes (ATP5MC3, DNAJC12, KMT2B, TBC1D24, TMEM151A); however, these signals were driven by small numbers of variants and were not robust to leave-one-variant-out analyses. CONCLUSIONS Rare variants in dystonia-related genes are not major contributors to overall PD risk. Signals observed in the EOPD subset require replication in larger cohorts. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

S. Kanagasingam, S. C. Parlar, Lang Liu et al. · 0 citations
Open access Jul 2026

Association Between Plasma Phosphorylated Tau-217 and Cognition in Parkinson's Disease.

BACKGROUND Alzheimer's disease (AD) co-pathology contributes to dementia in PD, but its role in earlier cognitive impairment remains uncertain. OBJECTIVE To determine if p-tau217, a biomarker of early AD, is associated with cognitive impairment in PD. METHODS Plasma p-tau217 levels in 167 PD patients without dementia and 63 controls were related to performance on standard neuropsychological testing, and to cognitive impairment as defined by a MoCA score <26 and by self-report. Plasma GFAP, NfL and APOE ε4 carrier status were also examined. RESULTS No significant differences in p-tau217, GFAP and NfL level were observed between groups (pFDR > 0.08). Higher p-tau217 was associated with worse visuospatial function and greater self-reported cognitive impairment, but these associations did not survive correction (pFDR > 0.08). There was no association with cognitive impairment (pFDR > 0.08). CONCLUSION These results suggest that co-morbid AD pathology is not a major contributor to early cognitive changes in this sample of PD patients without dementia. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

T. Kouchache, T. Chan, Sophie Sun et al. · 1 citation

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