Concepedia

Abstract

A clinical sample of 257 men were examined in a study of age-group differences on neurocognitive performance in adults with the Human Immunodeficiency Virus Type-1 (HIV-1). Older HIV-infected (HIV+) adults (M = 44.5 years) performed worse than younger HIV+ adults (M = 31.5 years) on a variety of neurocognitive tests. Similarly, HIV+ adults with the Acquired Immunodeficiency Syndrome (AIDS) performed worse than HIV+ adults without AIDS. Of greatest interest, age-group differences were larger in the AIDS group versus the No AIDS group. Brinley plot analyses show that the HIV+ adults presented minimal (or no) generalized cognitive slowing but that individual differences were systematically larger as a function of age and AIDS diagnosis. These results support both a brain reserve capacity model and a common-cause model of aging and HIV infection. Implications of aging and individual differences in HIV infection are discussed. Acquired Immunodeficiency Syndrome (AIDS) is a clinical syndrome resulting from the collapse of cell-mediated immunity secondary to infection with the Human Immunodeficiency Virus-Type 1 (HIV-1). The most common gross anatomical changes associated with AIDS include brain atrophy with sulcul widening and ventricular enlargement. Histopathological analyses reveal white matter abnormalities, multinucleated giant cells of macrophage origin, microglial nodules, and diffuse reactive astrocytosis to be present in 70 to 90% of the brains of patients with AIDS who come to autopsy. HIV often invades the central nervous system early in the course of infection producing a variety of neurocognitive symptoms. These include deficits in attention and concentration, abstraction, learning, memory, psychomotor and cognitive processing speed (Bornstein et al., 1993; Heaton et al., 1995; Hinkin, van Gorp, & Satz, 1995; McArthur & Seines, 1997). Symptom severity ranges from subtle psychomotor deficits to pronounced AIDS-related dementia (see Grant & Martin, 1994). It has become increasingly clear that the nature of the HIV epidemic is evolving, changing from a disease primarily affecting younger, gay White men to one affecting people of color, women, and the older adult. Indeed, the number of AIDS cases in adults over 50 years old has more than tripled in the last several years. Current estimates suggest that 10% of adults with AIDS are over 50 years old and about 3% are over 60 years old (CDC 1994, 1996; Chen et al., 1998; Shipp, Wolf, & Selik, 1991). This demographic shift is important because clinical outcomes are often worse in older adults with AIDS. The time between HIV infection and AIDS diagnosis (Phillips et al., 1991) and AIDS and death (Chen et al., 1998; Ferro & Salit, 1992; Gordon & Thomas, 1995; Shipp et al., 1991) is shorter in older adults compared to younger adults. Less clear is the neurocognitive prognosis of older adults with AIDS. Only a few studies have examined neurocognitive functioning in relation to HIV infection and aging. In a relatively large community sample (N = 199) of asymptomatic and symptomatic HIV-infected adults, Becker and colleagues (1997) found that test performance declined with age. This is noteworthy considering the mean age of the sample was 38 years with a standard deviation of 8.2 years. Performance also declined with age in HIV seronegative and seropositive adults in a large scale study by van Gorp and colleagues (1994). However, they did not find the effect of aging on standard test and reaction time performance to be different in HIV-positive adults compared to seronegative adults. In contrast, in an experimental study (Arendt, Hefter, Hilperath, & Strohmeyer, 1993) auditory event-related brain potentials (ERPs) were examined in 100 HIV-positive adults (mean age = 35 years) and 43 seronegative controls (mean age = 36 years). Amplitude of P300, an ERP component that has been linked to cognition (see Rugg & Coles, 1995), declined twice as fast with age in the HIV-infected adults relative to controls. …