The hypothesis is supported by the experimental proof of viral and bacterial infections being able to upregulate enteric α-synuclein [233] as well as by showing that repeated administration of an extracellular amyloid protein secreted by Escherichia coli (curli) to rats enhances neuronal deposition of α-synuclein in the gut and brain [234]. The gene discussed is SNCA; the disease is bacterial infectious disease.