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Updated: Jun 1, 2025
Detection of Disease-associated α-synuclein by Enhanced ELISA in the Brain of Transgenic Mice Overexpressing Human A53T Mutated α-synuclein
Published on: May 30, 2015
Toward alpha-synuclein seed amplification assay in clinical practice
Mathieu Verdurand1,2,3, Flora Kaczorowski1,2,3, Sophie Dautricourt2,4,5
1Biochemistry and Molecular Biology Department Neurodegenerative Pathologies LBMMS Hospices Civils de Lyon Lyon France.
Introduction:
Seed amplification assays (SAAs) demonstrate remarkable diagnostic performance in alpha-synucleinopathies. However, existing protocols lack accessibility in routine laboratories, mainly due to the requirement for in-house production of recombinant alpha-synuclein (aSyn). This study proposes a cerebrospinal fluid (CSF) aSyn-SAA protocol using solely commercial reagents to facilitate its clinical implementation.
Methods:
Routine clinical care CSF samples from 126 patients, comprising 47 with Lewy body diseases (LBD) (41 with dementia with Lewy bodies, six with Parkinson's disease), 37 without alpha-synucleinopathy, and 42 with Alzheimer's disease (AD), underwent assessment for aSyn-SAA activity.
Results:
CSF aSyn-SAA showed a sensitivity of 72.3% and a specificity of 100% when distinguishing clinically diagnosed LBD patients from those without alpha-synucleinopathy. In AD patients, 14.3% were tested positive for aSyn.
Discussion:
The commercial-only CSF aSyn-SAA protocol exhibited excellent specificity when applied to a real-life cohort, signaling progress toward the accessibility of an aSyn biomarker in clinical settings.
Highlights:
Diagnosis of LBD through aSyn-SAA lacks accessibility.This commercial-only aSyn-SAA has satisfactory performance in a real-life cohort.A negative aSyn-SAA does not completely exclude a synucleinopathy.Some technical points must be considered when developing aSyn-SAA.aSyn-SAA must be confined to expert laboratories due to prion-like risk management.
