University Medical Center Göttingen
Department of Neurology
Sandrina Weber graduated from the medical school of the Technical University of Munich. After one year of neurogenomics research, she began her neurology residency and research into biomarkers of parkinson’s disease at the Paracelsus-Elena-Klinik in Kassel, one of the largest specialized movement disorder clinics in Europe. Continuing both residency and research, she is currently a resident at the Department of Neurology, University Medical Center Goettingen.

Presenter of 1 Presentation

ALPHA-SYNUCLEIN SEED AMPLIFICATION ASSAY IN MANIFEST AND PRODROMAL PD FROM THE LONGITUDINAL DENOPA COHORT

Session Type
SYMPOSIUM
Date
Fri, 18.03.2022
Session Time
09:10 AM - 11:10 AM
Room
ONSITE: 114
Lecture Time
09:25 AM - 09:40 AM

Abstract

Aims

Diagnostic biomarkers are most valuable in the earliest stage of Parkinson’s disease (PD). Because of the high rate of misdiagnosis, early clinical diagnosis cannot be used as gold standard to evaluate accuracy of a diagnostic test. Our goal was to determine sensitivity and specificity of the αSyn Seed Amplification Assay (αS-SAA) for manifest and prodromal PD using the longitudinal DeNoPa cohort. Thus, we compared the αS-SAA results of baseline samples (collected weeks after diagnosis) versus their 8 year clinical diagnosis.

Methods

We blindly analyzed samples from 106 PD, 26 isolated REM sleep behavior disorder (iRBD), and 64 healthy controls (HC) patients. Patients were categorized based on baseline assessment and underwent biannual clinical follow-ups at a single center. CSF samples were analyzed in triplicate, using recombinant αSyn substrate. αS-SAA conditions used in this study have been described elsewhere.

Results

Of 90 (84,9%) patients with final PD diagnosis, 85 were αS-SAA-positive (94,4% sensitivity). 16 (15,1%) initially diagnosed PD cases changed clinically to other neurological disorders during follow-up, including 2 αS-SAA-positive MSAs. 62 HC were αS-SAA-negative (96,9% specificity). 24 (92,3%) iRBD patients were αS-SAA-positive, 8 of which converted to PD during follow-up.

Conclusions

αS-SAA enables the sensitive and specific detection of misfolded αSyn in early PD and iRBD. Compared to baseline clinical assessment (plus DATSCAN in most cases), αS-SAA was 13% more specific. Remarkably, CSF from iRBDs was αS-SAA-positive up to 8 years before phenoconversion to PD.

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