NFKB1 and Alzheimer disease: In support of this hypothesis, previous studies in hAPP transgenic mice have shown that the reduction of Sod2 activity accelerates the onset of AD-related behavioral deficits, alters amyloid deposition, worsens the severity of synaptic density deficits and neuritic dystrophy, enhances microgliosis and increases the activity of the redox-sensitive transcription factor NFκB in the brains of these mice.