All these LPS-mediated events are common in the brain of subjects affected by obesity and/or gut dysbiosis [8,58,59], wherein they culminate in several detrimental changes of synaptic plasticity ranging from impairment of memory formation networks in the hippocampus [60,61] to rapid refinement of dendritic spines and lowering of long-term potentiation (LTP) via IL1β-mediated enhancement of GABA tonic current at the GABA receptor [62,63]. This evidence concerns the gene IL1B and obesity disorder.