Amyloid β (Aβ) and tau are key hallmark features of Alzheimer's disease (AD) neuropathology. The interplay of Aβ and tau for cognitive impairment in early AD was examined with crosssectional analysis, measured by cerebrospinal fluid (CSF) biomarkers (Aβ1-42, total tau [t-tau] and phosphorylated tau [p-tau181P]), and on cognitive performance by the repeatable battery for assessment of neuropsychological status (RBANS). Participants (n=246) included cognitively normal (Aβ−), mild cognitively impaired (Aβ−), preclinical AD (Aβ+), and prodromal AD (Aβ+). Overall, cognitive impairment (RBANS Total Scale score) had a moderate negative correlation to t-tau (n=246; r=−0.434; p<0.001) and p-tau181P (r=−0.389; p<0.001). When classified by Aβ status, this correlation to t-tau was applicable only in Aβ+ participants (n=139; r=−0.451, p<0.001) but not Aβ− participants (n=107; r=0.137, p=0.16), with identical findings for p-tau. Both tau (p<0.0001) and interaction of Aβ1-42 with tau (p=0.006) affected RBANS, but not Aβ1-42 alone. Cognitive/memory performance correlated well with CSF tau levels across early stages of AD, although the correlation is Aβ dependent.