HIV-associated neurocognitive disorders: Five new things.

HIV-associated neurocognitive disorders (HAND) remain an important cause of cognitive dysfunction. Current nomenclature for HAND includes HIV-associated dementia and milder forms known as asymptomatic neurocognitive impairment (ANI) and mild neurocognitive disorder (MND). ANI and MND remain highly prevalent despite combined antiretroviral therapy (cART).

Developing neuroprotective strategies for treatment of HIV-associated neurocognitive dysfunction.

Important advances have been made in recent years in identifying the molecular mechanisms of HIV neuropathogenesis. Defining the pathways leading to HIV dementia has created an opportunity to therapeutically target many steps in the pathogenic process. HIV itself rarely infects neurons, but significant neuronal damage is caused both by viral proteins and by inflammatory mediators produced by the host in response to infection.

Ceftriaxone protects against the neurotoxicity of human immunodeficiency virus proteins.

Human immunodeficiency virus (HIV) proteins Tat and gp120 have been implicated in the pathogenesis of HIV dementia by various mechanisms, including down-regulation of excitatory amino acid transporter-2 (EAAT2), which is responsible for inactivation of synaptic glutamate. Recent work indicates that beta-lactam antibiotics are potent stimulators of EAAT2 expression. The authors treated mixed human fetal neuronal cultures with recombinant gp120 or Tat, in the presence or absence of ceftriaxone, and determined neurotoxicity by measuring mitochondrial membrane potential and neuronal cell death.

Viruses and the brain: from inflammation to dementia.

Many viruses cause encephalitis, but understanding the mechanisms by which viral infection leads to encephalopathy or dementia remain elusive. In many cases, inflammation generated by the host's attempt to combat the infection is itself implicated as a primary factor in causing neuronal dysfunction or degeneration. In this review, we outline the current state of knowledge regarding the pathophysiology of CNS (central nervous system) injury in viral infection.

Developments in HIV neuropathogenesis.

Despite the fact that neurons are rarely infected by the human immunodeficiency virus (HIV), neuronal loss is common in patients with HIV infection, likely due to the effects of viral proteins and inflammatory mediators on these cells. Despite the widespread use of highly active antiretroviral therapy (HAART), at least in developed nations, cognitive impairment and other neurological complications of HIV infection persist with devastating personal and socioeconomic consequences. Fortunately, we have made important advances in recent years in defining the molecular mechanisms by which HIV infection targets the nervous system for damage.

Pseudomonas aeruginosa infective endocarditis presenting as bacterial meningitis.

Pseudomonas aeruginosa is a rare cause of infective endocarditis. The case of community-acquired P. aeruginosa infective endocarditis reported here is the first described in the literature to present as bacterial meningitis.