The incorporation of additional biomarkers that are likely to discriminate early AD from cognitive normalcy, such as those identified in the first phase of this study, or other biomarkers that have already shown promise for distinguishing AD from other leading causes of dementia (e.g. agouti related peptide, eotaxin-3, and hepatocyte growth factor [19], complement C3a des-arg and integral membrane protein 2B CT [22], for FTLDs; and alpha-synuclein [228], apoH and vitamin D binding protein [25] for Lewy body disorders), would likely improve the panel's diagnostic utility. This evidence concerns the gene CCL26 and Alzheimer disease.