VIP receptor binding in the frontal cortex, a region with substantial neuronal loss, was unaltered in individuals who had died of acquired immunodeficiency syndrome (AIDS) neurotoxicity. In contrast, ascorbic acid, which suppresses human immunodeficiency virus (HIV) replication and modulates glutamatergic neuronal activity, was reduced by nearly 60% in the same brain region. These findings indicate that while neurons containing ascorbic acid may be lost, vasoactive intestinal polypeptide (VIP) receptor bearing cells remain viable. This finding supports previous observations that VIP prevents HIV induced neuronal death. The reduced ascorbic acid levels may contribute to particular neurons being vulnerable to damage from oxidative stress and possibly clinically to the development of dementia.