Parkinsonism & related disorders · 2026
Differential patterns of central synucleinopathy and catecholaminergic abnormalities in Lewy body diseases and multiple system atrophy.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод в очереди
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Goldstein David S, Concha-Marambio Luis, Alam Parvez, Sullivan Patti, Holmes Courtney, Bloch Miriam, Hughson Andrew G, Caughey Byron
Аннотация
INTRODUCTION: Parkinson's disease (PD), pure autonomic failure (PAF), and multiple system atrophy (MSA) feature intracellular deposition of alpha-synuclein and catecholamine deficiency in the putamen or heart. This retrospective, cross-sectional, observational study assessed relationships of cerebrospinal fluid alpha-synuclein seed amplification assay (CSF SAA) data with catecholamine deficiency indicated by positron emission tomography (PET).
METHODS: In groups with PD, PAF, parkinsonian MSA (MSA-P), or cerebellar MSA (MSA-C) SAAs were conducted by Rocky Mountain Laboratories (RML) and Amprion, Inc. using different assay conditions. 18F-DOPA PET examined putamen dopaminergic innervation, and 18F-dopamine PET assessed cardiac noradrenergic innervation.
RESULTS: CSF SAAs by both RML and Amprion separated PD or PAF from MSA. The Amprion assay detected type 1 seeding associated with Lewy body diseases (LBDs) in 22/24 (92%) PD patients and 15/16 (94%) PAF patients and type 2 seeding associated with MSA in 9/10 (90%) MSA-P and 3/4 (75%) MSA-C patients (p < 0.0001). All of 24 PD and all of 9 MSA-P patients had low putamen/occipital cortex ratios of 18F-DOPA-derived radioactivity, while 11/13 (85%) PAF patients and 4/4 (100%) MSA-C patients had normal ratios. Contingency analyses of CSF SAA and brain 18F-DOPA PET efficiently separated the 4 groups (p < 0.0001).
CONCLUSION: CSF SAAs and cardiac 18F-dopamine PET distinguish LBDs from MSA but not PAF from PD or MSA-P from MSA-C. 18F-DOPA PET separates PAF from PD and MSA-P from MSA-C. Combining biomarkers differentiates among these synucleinopathies.
METHODS: In groups with PD, PAF, parkinsonian MSA (MSA-P), or cerebellar MSA (MSA-C) SAAs were conducted by Rocky Mountain Laboratories (RML) and Amprion, Inc. using different assay conditions. 18F-DOPA PET examined putamen dopaminergic innervation, and 18F-dopamine PET assessed cardiac noradrenergic innervation.
RESULTS: CSF SAAs by both RML and Amprion separated PD or PAF from MSA. The Amprion assay detected type 1 seeding associated with Lewy body diseases (LBDs) in 22/24 (92%) PD patients and 15/16 (94%) PAF patients and type 2 seeding associated with MSA in 9/10 (90%) MSA-P and 3/4 (75%) MSA-C patients (p < 0.0001). All of 24 PD and all of 9 MSA-P patients had low putamen/occipital cortex ratios of 18F-DOPA-derived radioactivity, while 11/13 (85%) PAF patients and 4/4 (100%) MSA-C patients had normal ratios. Contingency analyses of CSF SAA and brain 18F-DOPA PET efficiently separated the 4 groups (p < 0.0001).
CONCLUSION: CSF SAAs and cardiac 18F-dopamine PET distinguish LBDs from MSA but not PAF from PD or MSA-P from MSA-C. 18F-DOPA PET separates PAF from PD and MSA-P from MSA-C. Combining biomarkers differentiates among these synucleinopathies.