Although we have not directly explored the impact of increased Cx43-HC activity as a trigger of memory dysfunction, this increased of Cx43 might be a contributing factor for AD-related dysfunction of synaptic plasticity and memory since the genetic silencing of Cx43 affords a neuroprotection against Aβ-induced modifications [55] and improves memory deficits in APP/PS1 mice by increasing synaptic function without affecting amyloid plaque formation or the inflammatory response [18, 59]. The gene discussed is GJA1; the disease is amyloidosis.