Human immunodeficiency virus-1 (HIV-1) andToxoplasma gondiican invade the central nervous system and affect its functionality. Advanced HIV-1 infection has been associated with defects in immune response toT.gondii, leading to reactivation of latent infections and development of toxoplasmic encephalitis. This study evaluates relationship between changes in immune response toT.gondiiand neurocognitive impairment in HIV-1/T.gondiico-infected patients, across different stages of HIV-1 infection. The study assessed the immune response toT.gondiiby measuring cytokine production in response to parasite antigens, and also neurocognitive functions by performing auditory and visual P300 cognitive evoked potentials, short term memory (Sternberg) and executive function tasks (Wisconsin Card Sorting Test-WCST) in 4 groups of individuals: HIV-1/T.gondiico-infected (P2), HIV-1-infected/T.gondii-non-infected (P1), HIV-1-non-infected/T.gondii-infected (C2) and HIV-1-non-infected/T.gondii-non-infected (C1). Patients (P1 and P2) were grouped in early/asymptomatic (P1A and P2A) or late/symptomatic (P1B/C and P2B/C) according to peripheral blood CD4+ T lymphocyte counts (>350 or <350/μL, respectively). Groups were compared usingT-studentorU-Mann-Whitneytests as appropriate,p<0.05was considered as significantly. For P300 waves, HIV-1-infected patients (P1) had significantly longer latencies and significantly smaller amplitudes than uninfected controls, but HIV-1/T.gondiico-infected patients (P2) had significantly longer latencies and smaller amplitude than P1. P1 patients had significantly poorer results than uninfected controls in Sternberg and WCST, but P2 had significantly worse results than P1. HIV-1 infection was associated with significantly lower production of IL-2, TNF-α and IFN-γ in response toT.gondiifrom early/asymptomatic stages, when comparing P2 patients to C2 controls. These findings may indicate impairment in anti-parasitic response in co-infected patients, facilitating early limited reactivation of the parasitic latent infection, therefore creating cumulative damage in the brain and affecting neurocognitive functions from asymptomatic stages of HIV-1 infection, as suggested by defects in co-infected patients in this study.