NFKB1 and Parkinson disease: The shared disruptions of brain cells’ signalling pathways in T2D and PD are due to attenuated PI3K-AKT signalling pathway activity, which is the result of impaired insulin signalling, leading to (a) the FOXO1-promoted activation of pro-apoptosis factors and reduced MT function [2,235,237,351]; (b) GSK3-increased α-syn aggregation, NF-κB-enhanced NLRP3 inflammasome activation, pro-inflammatory cytokine signalling ((IL)-1β, -6; TNFα), and pro-inflammatory microglial activation [2,235,237]; and (c) reduced neural growth and synaptic plasticity or cell death due to mTOR inhibition [2,235,237].