Alzheimer’s disease (AD) is characterized by progressive neurodegeneration in the cerebral cortex, histopathologically hallmarked by amyloid β (Aβ) extracellular plaques and intracellular neurofibrillary tangles, constituted by hyperphosphorylated Tau protein. Correlation between these pathological features and dementia has been challenged by the emergence of "Non-Demented with Alzheimer’s Neuropathology" (NDAN) individuals, cognitively intact despite displaying pathological features of AD. The existence of these subjects suggests that some unknown mechanisms are triggered to resist Aβ-mediated detrimental events. Aβ accumulation affects mitochondrial redox balance, increasing oxidative stress status, which in turn is proposed as a primary culprit in AD pathogenesis. To clarify the relationship linking Aβ, oxidative stress and cognitive impairment, we performed a comparative study on AD, NDAN and aged-matched human post-mortem frontal cortices of either sex. We quantitatively analyzed immunofluorescence di...