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Alpha-synuclein seeding activity in postmortem tissues from patients with diffuse and isolated Lewy bodies
Soňa Baranová1, Radoslav Matěj2,3,4, Jakub Soukup1
1Institute of Medical Microbiology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
Acta Neuropathologica Communications
|January 8, 2026
Summary
The seeding amplification assay (SAA) effectively detects alpha-synuclein in brain and CSF, showing high sensitivity for synucleinopathies. This assay aids in diagnosing co-pathologies, including Lewy body presence in Alzheimer's disease cases.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Alpha-synucleinopathies are a group of neurodegenerative diseases characterized by the abnormal aggregation of alpha-synuclein protein.
- Distinguishing between primary synucleinopathies and those with co-pathologies, such as Alzheimer's disease, is diagnostically challenging.
- Accurate detection of alpha-synuclein seeding activity is crucial for understanding disease mechanisms and progression.
Purpose of the Study:
- To evaluate the diagnostic performance of the seeding amplification assay (SAA) for detecting alpha-synuclein seeding activity.
- To assess SAA's utility in postmortem brain and cerebrospinal fluid (CSF) samples from patients with primary and co-pathology alpha-synucleinopathies.
- To investigate potential SAA positivity in control samples that might indicate unrecognized co-pathology.
Main Methods:
- Utilized the seeding amplification assay (SAA) with recombinant wild-type alpha-synuclein (WT) with an N-terminal His-tag.
- Tested postmortem brain and CSF samples from patients diagnosed with dementia with Lewy bodies (DLB), Alzheimer's disease with amygdala Lewy body (AD/ALB), and Creutzfeldt-Jakob disease with Lewy body pathology (CJD/LBP).
- Included control samples from other neurodegenerative diseases and healthy corneal donors.
Main Results:
- SAA demonstrated 100% sensitivity and 91.2% specificity in brain samples.
- SAA showed 100% sensitivity and 94.4% specificity in CSF samples, with some requiring dilution due to inhibitors.
- Five control brain samples were initially positive; two were reclassified as Alzheimer's disease with synucleinopathy co-pathology upon reevaluation.
Conclusions:
- The seeding amplification assay (SAA) performs well in detecting alpha-synuclein seeding activity in postmortem samples.
- SAA is effective for both primary synucleinopathies and co-pathology cases, including those with isolated Lewy bodies in Alzheimer's disease.
- The findings underscore the importance of careful diagnostics to identify co-existing synucleinopathy in Alzheimer's disease patients.
