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Loading metrics Open Access Peer-reviewed Research Article Huei-Chun Liu, Wei-Che Lin, Ming-Jang Chiu, Cheng-Hsien Lu, Chin-Yi Lin, Shieh-Yueh Yang Huei-Chun Liu, Wei-Che Lin, Ming-Jang Chiu, Cheng-Hsien Lu, Chin-Yi Lin, Shieh-Yueh Yang Published: June 12, 2020 https://doi.org/10.1371/journal.pone.0234519 Figures Abstract Axonal damage leads to the release of neurofilament light chain (NFL), which enters the CSF or blood.

Introduction Atypical parkinsonism syndrome (APS), including multiple system atrophy (MSA), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), dementia with Lewy body (DLB), and frontotemporal dementia (FTD) with parkinsonism (FTD-P), have a large clinical overlap with Parkinson’s disease (PD). However, the treatment response to levodopa and prognosis are distinct in patients with PD and APS (Bower et al., 1997; Elbaz et al., 2003).

We previously developed an ultra-sensitive immunoassay utilising immunomagnetic reduction (IMR), 13 14 which could quantitatively detect biomolecules at ultra-low concentrations with a fg/mL limit of detection. This would theoretically facilitate measurements of plasma ?-synuclein from control subjects and patients with PD.