The scrapie prion protein (PrP Sc) has been shown to induce apoptosis of rat cortical neurons in vitro. Here we demonstrate that the toxic effect displayed by PrP Sc can be blocked by sulfated colominic acid (polymer of N-acetylneuraminic acid). This compound acts neuroprotectively at a concentration of 50.3 mg/ml when preincubated with the neurons or PrP Sc. Rat cortical cells also undergo apoptosis after incubation with the HIV-1 coat protein gp120 in vitro. This effect was abolished also by sulfated colominic acid when preincubated with the cells or gp120. Addition of 0.3 mg/ml of compound resulted in an increase in cell viability by about 1.6 ± 1.9-fold compared to cultures incubated for 18 h with 30 ng/ml of PrP Sc or 20 ng/ml of gp120 alone (containing about 40% viable cells). Sulfated colominic acid does not act as antagonist of NMDA receptor channels at concentrations of up to 3 mg/ml when co-administered with 100 mg/ml of NMDA. It displayed a strong cytoprotective effect on human T lymphoblastoid CEM cells exposed to HIV-1; a 50 % protection occurred after preincubation of the cells with 0.43 mg/ml of compound. At the same concentration, the compound caused an inhibition of HIV-1-induced syncytium formation. Sulfated colominic acid may be a promising compound for treatment of dementia caused by PrP Sc and HIV-1 infections
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