α-Synuclein orchestrates Th17 responses as antigen and adjuvant in Parkinson's disease.

Recently, the role of T cells in the pathology of α-synuclein (αS)-mediated neurodegenerative disorders called synucleinopathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy, has attracted increasing attention. Although the existence of αS-specific T cells and the immunogenicity of the post-translationally modified αS fragment have been reported in PD and DLB, the key cellular subset associated with disease progression and its induction mechanism remain largely unknown.Peripheral blood mononuclear cells (PBMCs) from synucleinopathy patients and healthy controls were cultured in the presence of the αS peptide pools.

Propagative α-synuclein seeds as serum biomarkers for synucleinopathies.

Abnormal α-synuclein aggregation is a key pathological feature of a group of neurodegenerative diseases known as synucleinopathies, which include Parkinson's disease (PD), dementia with Lewy bodies and multiple system atrophy (MSA). The pathogenic β-sheet seed conformation of α-synuclein is found in various tissues, suggesting potential as a biomarker, but few studies have been able to reliably detect these seeds in serum samples. In this study, we developed a modified assay system, called immunoprecipitation-based real-time quaking-induced conversion (IP/RT-QuIC), which enables the detection of pathogenic α-synuclein seeds in the serum of individuals with synucleinopathies.