Changes in emotional response towards different facial application gestures following skincare application: An electroencephalogram approach.

Misfolded, aggregated alpha-synuclein (αSyn) is the pathological hallmark of clinically heterogeneous neurodegenerative diseases including Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). In histopathologically confirmed cases of PD and DLB, aggregated αSyn is found in neuronal inclusions called Lewy bodies (LB), whereas MSA is characterized by oligodendroglial inclusions of αSyn. PD and DLB have been referred to as neuronal synuclein diseases (NSD). In all NSD, aggregates can be found in prodromal stages, before the onset of cardinal symptoms. Prion-like properties of αSyn aggregates contribute to the spread of pathology throughout the nervous system, causing motor- and non-motor symptoms. In this process, an aggregation nucleus or seed induces the conversion of unfolded α-Syn molecules towards pathological aggregates. These properties are exploited in seed amplification assays (SAA) to detect minute amounts of αSyn seeds in biomaterials such as cerebrospinal fluid (CSF). An early and accurate diagnosis of neurodegenerative diseases is required for life and care planning, monitoring of disease progression, and potentially for therapeutic decisions. For this reason, definitions of neurodegenerative diseases increasingly include biomarkers such as the αSyn-SAA. To date, the performance of αSyn-SAA in CSF has been studied extensively in well-characterized cohorts with PD, DLB, MSA, dementia and REM sleep behavior disorder (RBD). Yet, results from well-characterized cohorts only allow limited conclusions about the diagnostic value of a fluid biomarker in a clinical setting, because cohorts only include patients with specific diseases whereas a much broader range of diagnoses is observed in clinical routine.