APP and Alzheimer disease: Since we showed that elevating either APP or Aβ in WT neurons can increase neuronal activity, we hypothesized that the continuously high levels of APP and Aβ in APP/PS1 neurons disrupt neuronal network activity and function, and speculated that HSP mechanisms, which help maintain synaptic firing within the boundaries of meaningful communication (Turrigiano, 2008), might be impaired in AD transgenic neurons and, as a result, may no longer be effective at returning activity levels back to a baseline.