The diagnostic discrimination of cutaneous α-synuclein deposition in Parkinson disease  

Results: Skin biopsies provide >90% sensitivity and >90% specificity to distinguish PD from control participants across all biopsies sites with quantification of either pilomotor or sudomotor α-synuclein deposition. All individuals with PD have significantly higher cutaneous α-synuclein deposition than control participants, even those individuals with PD and no evidence of autonomic dysfunction. Deposition of α-synuclein is most prominent in sympathetic adrenergic nerve fibers innervating the arrector pili muscles, but is also present in sudomotor (sympathetic cholinergic) nerve fibers. α-Synuclein is present even in the early stages of disease and disease of short duration. α-Synuclein ratios were higher in individuals with autonomic failure, with more advanced stages of disease and disease of longer duration.Conclusions: The α-synuclein ratio provides a sensitive and specific diagnostic biomarker of PD even in patients without autonomic failure.Classification of evidence: This study provides Class III evidence that cutaneous α-synuclein deposition accurately identifies patients with PD.

Source: The diagnostic discrimination of cutaneous α-synuclein deposition in Parkinson disease – PMC


  • So seems that sweat glands are secreting alpha-synuclein, could sweating be used to detox or to normalize levels of alpha-synuclein

Could α-Synuclein Inhibition be a Treatment for PD?

A 2020 publication in the MDPI journal, Biomolecules looks at targeting a-syn for PD therapeutics. PD is characterized by the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy Bodies (cytoplasmic inclusions). The Lewy Bodies are clumps of protein that can build up and create problems in the brain. The Lewy Bodies contain the aggregated a-synuclein protein that can propagate throughout the brain. Many PD studies have looked at ways of inhibiting a-synuclein accumulation to ease PD symptoms. There are various approaches to a-syn inhibition and multiple clinical trials that examine the link between PD and a-syn, with the hope that a treatment may be found for PD using a-syn. Given the central role of α-syn in PD pathology and progression, α-syn met the criteria to be a tantalizing and evident therapeutic target for PD. Promising strategies include predominantly immunization, anti-aggregative molecules, and an increase in α-syn clearance.

Source: Targeting α-Synuclein for PD Therapeutics: A Pursuit on All Fronts