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Although the trigger that contributes to fibrillization and pathological cross-seeding curli protein is unclear, a genome-wide screening analysis identified that bacterial curli amyloid was the distinguishing factor for prompting cross-seed -synuclein aggregation and dysfunction of mitochondrial cellular respiration in both an in vitro neuroblastoma cell line and in vivo A53T -synuclein over-expressing C
It has a key role in the normal functioning of the brain and nervous system, and for the formation of blood
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This process is mediated by mast cells, as the neurotransmitters released by peripheral neurons induce mast cell degranulation and the release of additional proinflammatory mediators
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