Twenty-five percent of elders whose neuropsychological testing is unimpaired prior to death meet full pathologic criteria for AD (Ince 2001), suggesting that this degree of pathology does not invariably result in clinical dementia. Educational and occupational exposure and leisure activities are considered Inhibitors,research,lifescience,medical that as related with a reduced risk of developing dementia (Stern 2009). Neuropathologic correlations support this theory showing that individuals with greater cognitive reserve, as reflected in years of education, are
better able to cope with AD brain pathology without observable cognitive deficits (Roe et al. 2007). However, results from studies examining the relation of the education level with other than the clinical onset aspects, such as the rate of cognitive Inhibitors,research,lifescience,medical decline, were not consistent. In a study of AD patients with mild or moderate stage, higher educational attainment was associated with a slower rate of cognitive decline on the Mini-Mental State Exam (MMSE) (Fritsch et al. 2001). Another study showed that higher educational attainment was associated with a slightly accelerated Inhibitors,research,lifescience,medical rate of cognitive deterioration (Wilson et al. 2009). Data analysis of a large cohort of participants in the Victoria Longitudinal Study
showed that years of education were strongly related to cognitive level in all domains, particularly verbal fluency, but education Inhibitors,research,lifescience,medical was not related to rates of change over time for any cognitive domain (Wilson et al. 2004). In a prospective community survey in
old subjects without an established clinical diagnosis of AD, education was robustly associated with level Inhibitors,research,lifescience,medical of cognitive function but not with the rate of cognitive decline (Zahodne et al. 2011). A meta-analysis of data of 34 previously published studies showed that education, hypertension, CXCR antagonist objective indices of health, cardiovascular disease, and apolipoprotein E (APOE) were associated with cognitive decline in old-age subjects (Anstey and Christensen 2000). As mild cognitive impairment (MCI) is a clinically and pathologically heterogeneous state, showing a conversion rate into dementia of 11-33% within 3-mercaptopyruvate sulfurtransferase 2 years (Gauthier et al. 2006) or approximately 12% per year (Petersen et al. 1999; Anchisi et al. 2005), the question about the appliance of the cognitive reserve theory in MCI has probable conflicting answers. Recent investigations based on neuroimaging measurements (Solé-Padullésa et al. 2009), biochemical methods (Rolstad et al. 2010), and epidemiological studies (Afgin et al. 2012) were indicative that the cognitive reserve hypothesis may be applied also in MCI subjects.