AIDS dementia complex (ADC; also known as HIV dementia, HIV encephalopathy and HIV-associated dementia) is a common neurological disorder associated with HIV infection and AIDS. It is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of brain macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of ADC are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal apoptosis.
ADC typically occurs after years of HIV infection and is associated with low CD4+ T cell levels and high plasma viral loads. It is sometimes seen as the first sign of the onset of AIDS. Prevalence is between 10-20% in Western countries and has only been seen in 1-2% of India based infections. This may have to do with differences in diets, such as consumption of curcumin (in curry) and EGCG or Theaflavins (in teas), both which can pass the blood brain barrier and have neuroprotective effects. With the advent of highly active antiretroviral therapy (HAART), the frequency of ADC has declined in developed countries. HAART may not only prevent or delay the onset of ADC in people with HIV infection, it can also improve mental function in people who already have ADC.
Dementia only exists when neurocognitive impairment in the patient is severe enough to interfere markedly with day-to-day function. That is, the patient is typically unable to work and may not be able to take care of him or herself. Before this, the patient is said to have a mild neurocognitive disorder.
While the progression of dysfunction is variable, it is regarded as a serious complication and, untreated, can progress to a fatal outcome. Diagnosis is made by neurologists who carefully rule out alternative diagnoses. This routinely requires a careful neurological examination, brain scans (MRI or CT scan) and a lumbar puncture to evaluate the cerebrospinal fluid. No single test is available to confirm the diagnosis, but the constellation of history, laboratory findings, and examination can reliably establish the diagnosis when performed by experienced clinicians. The amount of virus in the brain does not correlate well with the degree of dementia, suggesting that secondary mechanisms are also important in the manifestation of ADC.
Many researchers believe that HIV damages the vital brain cells, neurons, indirectly. According to one theory, HIV either infects or activates cells that nurture and maintain the brain, known as macrophages and microglia. These cells then produce toxins that can set off a series of reactions that instruct neurons to kill themselves. The infected macrophages and microglia also appear to produce additional factors chemokines and cytokines - that can affect neurons as well as other brain cells known as astrocytes. The affected astrocytes, which normally nurture and protect neurons, also may now end up harming neurons. The HIV virus protein gp120 inhibits the stem cells in the brain from producing new nerve cells. Researchers hope that new drugs under investigation will interfere with the detrimental cycle and prevent neuron death.