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Description
Alzheimer’s disease (AD) biomarkers indicate who is at risk for developing the disease, facilitate early diagnosis and can inform research to discover treatment options. Apolipoprotein E (ApoE) genotype, ß-amyloid (Aß), tau, hippocampal volume, entorhinal thickness, and olfactory impairment are known biomarkers of AD; however, no single biomarker can predict AD on its own. Cognitive reserve has gained recognition due to its ability to alter neural networks, compensating for pathology. Therefore, this study investigated the protective effects of cognitive reserve and assessed it as a biomarker of AD. Neuropsychological tests, AD biomarkers and neuroimaging aimed to uncover how these markers predict cognitive impairment. Archival de-identified data from nondemented adults 75 years or older was analyzed in this study. Cognitive reserve was operationally defined as self-reported years of education. The ADAS-Cog-Odor, a novel add-on test, was administered in the context of the ADAS-Cog-13 by including an odor-place association task. Separate ADAS-Cog-Odor and ADAS-Cog-13 scores were analyzed to identify the best measure of cognitive impairment. Olfactory function was operationally defined as the combined activation in the left hippocampus and entorhinal cortex during odor identification and familiarity. Additionally, neuroimaging was used to obtain data on hippocampal volume and entorhinal cortex thickness. A correlation analysis found that entorhinal cortex thickness was significantly correlated only with low olfactory function, which has been associated with preclinical AD, and is typically seen before hippocampal atrophy. Hippocampal volume, a hallmark pathology of AD, was significantly associated with the ADAS-Cog-Odor. Cognitive reserve was significantly associated with ADAS-Cog-13. Four regression analyses were used to discover the predictive ability of cognitive reserve, gender, and the listed AD biomarkers. A combination of markers was more predictive than individual markers. The sample was limited by size and range of years of education, thus these findings are preliminary; however, they strongly suggest that early brain pathology in the AD cascade is reflected in olfactory function and the ADAS-Cog-Odor. Future work will investigate whether the ADAS-Cog or the ADAS-Cog-Odor is a better predictor of conversion to MCI or AD. The current work suggests that gender and cognitive reserve may influence that prediction.
