ABSTRACT
The Melbourne Aging Study arose from our observations of the dissociation between the progressive nature of the biochemical and clinical manifestations of Alzheimer's disease (AD), and the criteria for diagnosing AD in its earliest stages. Our review of the criteria for mild cognitive impairment (MCI) identified that while all criteria required objective evidence of a cognitive deficit, none required objective evidence of cognitive decline (Collie & Maruff, 2002a). This is inconsistent with neuropathological evidence for a long prodromal period in the AD process (Price & Morris, 1998), during which time aspects of cognition, particularly memory, demonstrate progressive deterioration (Collie & Maruff, 2000; Elias, Beiser, Wolf, Au, White, & D'Agostino, 2000). At the same time, we were aware that prospective studies of individuals classified as having MCI were reporting conversion to AD of only approximately 50% over 5–10 years (Bowen, Tcri, Kukull, McCormick, McCurry, & Larson, 1997; Hanninen, Hallikainen, Koivisto Helkala, Reinikainen, & Soininen et al., 1995). Further, studies that challenged groups of MCI patients with other putative risk factors for AD were reporting conflicting results. For example, there was disagreement regarding the proportion of older individuals with MCI who carry the apolipoprotein E epsilon 4 (ApoE–4) allele, a genetic predictor of late onset sporadic AD (Reed et al., 1994; Smith et al., 1998). When considered together, these findings suggested that criteria for MCI based on a single assessment, aimed at identifying dysfunction or impairment, were inaccurate predictors of conversion to AD. Our hypothesis was that a more potent predictor of risk for developing AD was evidence of cognitive, particularly memory, decline demonstrated objectively. The Melbourne Aging Study was designed to address this hypothesis.
