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Patients with more severe disease have higher levels of S2-, S1-, and RBD-binding antibodies and concomitantly the strongest serum nAb titers at two to four weeks after infection [85]

Vergauwen, B., Elegheert, J., Dansercoer, A., Devreese, B

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These include mutations in genes such as: SNCA Alpha-synuclein gene PRKN Parkin RBR E3 Ubiquitin Protein Ligase PINK1 Gene PARK6 DJ-1 and PARK7 Gene LRRK2 It is believed that mutations in these genes can cause dysfunction and eventual death of dopamine-producing neurons through various mechanisms, including protein aggregation, mitochondrial dysfunction, and oxidative stress

Elevated CSF and plasma PM levels and dried blood spot assays showing reduced PNPO enzyme activity are hallmarks of PNPO gene mutations [14]