rather the result of the common neuropathologies that ultimately result in MCI and dementia [198]. This conclusion is consistent with reports that AD pathology is common among persons with MCI [199–202] and some report AD pathology among persons without cognitive impairment [203–208]. We related AD pathology to subtle decrements in episodic memory among persons without cognitive impairment [154]. These data are consistent with what is being reported with amyloid imaging agents among persons without dementia but are based on quantitative neuropathologic data [209,210]. Overall, the data suggest that there is unlikely to be qualitatively meaningful biologic distinctions between MCI and AD, regardless of the definition used. The data strongly support the recent revised criteria of AD as beginning with a pathophysiologic process and evolving to MCI due to AD and finally to AD dementia [211–213].
