Selective pharmacological activation of GABAA receptors has been shown to provide neuroprotection against Aβ mediated toxicity [58–60], and the GABA-potentiating [60, 61] and anti-TNF-α [62, 63] properties of CMZ are of clinical utility in AD; nevertheless, we hypothesized that it was essential also to address synaptic dysfunction [64, 65]. The gene discussed is TNF; the disease is Alzheimer disease.