Objective: Several studies have shown a link between HIV and Alzheimers dementias (HAD) (AD). There is increasing evidence that CSF levels of amyloid beta 1-42 (AB), t-tau, and p-tau can be used as ancillary tools for AD diagnosis and prediction. We sought to determine whether these markers were abnormal in patients with and without ADC. Methods: CSF samples from cohorts of patients in Sydney, Gotheborg, Milan and San Francisco were accessed. All patients had been neurologically evaluated and investigated as appropriate. HAD was diagnosed according to AAN criteria. CSF AB, t-tau and CSF p-tau levels were measured using an ELISA (Innogenetics). The lower limit of detections were: t-tau 75pg/ml, p-tau 16pg/ml and AB 20pg/ml. HIV negative out-of-hospital controls were used and a cohort of AD patients. Results: For the AB analyses there were 120 patients without HAD, 47 with stage 1 and 62 with stage 2; for p-tau there were 103, 20 and 40 patients while for t-tau there were 121, 45 and 49 patients. CSF AB levels were significantly reduced in HAD and t-tau levels increased compared to both the non demented group and HIV negative controls. The HAD group did not differ from the AD group. CSF p-tau concentrations however were not raised. Conclusions: That CSF AB and t-tau levels were abnormal in HAD and not different from AD points to similarities in basic pathogenetic mechanisms. However, the finding of normal CSF p-tau in HAD strongly suggests that it may be useful in differentiating the two conditions.