This hypercortisolaemic state further primes microglialTLR4/NF-κB pathway activation, ultimately inducing neuronal apoptosis.Qiu et al. [52] identified associations between cognitive dysfunctionand increased serum TG levels in patients with bipolar disorder throughglucose-lipid metabolism assessments—a finding divergent from the observationof “no significant TG level differences across cognitive function groups”. This evidence concerns the gene NFKB1 and bipolar disorder.