GAD1 and Alzheimer disease: Studies have shown a similar yet lower degree of various GABAergic component alterations, including depression of GABA levels [39], increased GAD activity [37], synaptic function disruption at GABAergic terminals [37], and increased sensitivity of GABA receptors [73], indicating the lack of inhibitory responses in subcortical regions such as the thalamus, Locus Coeruleus (LC), cochlear, and vestibular nucleus compared to cortical regions during the AD pathology or aged brain.