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Alcohol use is a risk factor for nonadherence to antiretroviral therapy (ART) among people living with HIV/AIDS (PLWHA); however, differences in ART adherence across levels of alcohol use are unclear. This study examined whether “at‐risk” alcohol use, defined by National Institute of Alcohol Abuse and Alcoholism guidelines, was associated with ART nonadherence among PLWHA. Participants were 535 HIV‐infected adults enrolled in studies at the HIV Neurobehavioral Research Program. ART nonadherence was identified by either self‐reported missed dose or plasma viral load detectability (≥50 copies/ml). Potential covariates for multivariable logistic regression included demographics, depression, and substance use disorders. Using a stepwise model selection procedure, we found that at‐risk alcohol use (OR = 0.64; p= 0.032) and low education (OR = 1.09 per 1 year increase in education; p= 0.009) significantly predict lower ART adherence. A greater focus on the treatment of at‐risk alcohol use may improve ART adherence among HIV‐infected persons. In a sample of 535 HIV‐infected adults, at‐risk alcohol drinkers (defined as >3 drinks per day for women, and >4 drinks per day for men) were significantly more likely to be non‐adherent to their antiretroviral therapy (ART) medication than not at‐risk drinkers. These findings suggest that a greater emphasis on treatments designed to reduce heavy alcohol use among persons living with HIV may, in turn, help with ART adherence and ultimately improve quality of life for these individuals.

The acute consumption of excessive quantities of alcohol causes well‐recognized neurophysiological and cognitive alterations. As people reach advanced age, they are more prone to cognitive decline. To date, the interaction of current heavy alcohol (ethanol [EtOH]) consumption and aging remains unclear. This study tested the hypothesis that negative consequences of current heavy alcohol consumption on neurocognitive function are worse with advanced age. Further, we evaluated the relations between lifetime history of alcohol dependence and neurocognitive function Sixty‐six participants underwent a comprehensive neurocognitive battery. Current heavy EtOH drinkers were classified using National Institute on Alcohol Abuse and Alcoholism criteria (EtOH heavy, n= 21) based on the Timeline follow‐back and a structured clinical interview and compared to nondrinkers, and moderate drinkers (EtOH low, n= 45). Of the total population, 53.3% had a lifetime history of alcohol dependence. Neurocognitive data were grouped and analyzed relative to global and domain scores assessing: global cognitive function, attention/executive function, learning, memory, motor function, verbal function, and speed of processing. Heavy current EtOH consumption in older adults was associated with poorer global cognitive function, learning, memory, and motor function (ps < 0.05). Furthermore, lifetime history of alcohol dependence was associated with poorer function in the same neurocognitive domains, in addition to the attention/executive domain, irrespective of age (ps < 0.05). These data suggest that while heavy current alcohol consumption is associated with significant impairment in a number of neurocognitive domains, history of alcohol dependence, even in the absence of heavy current alcohol use, is associated with lasting negative consequences for neurocognitive function. As we age, our susceptibility to negative consequences of heavy alcohol consumption for thinking, memory, and motor skills appears to increase. While there were no significant cognitive differences evident in younger adults that did and did not drink heavily, current heavy alcohol consumption in older adults was associated with significantly poorer cognitive function in learning, memory, and speeded motor function, as well as a global marker of cognition.

To examine whether depression and apathy are independently associated with longitudinal trajectories of cortical atrophy in the entorhinal cortex compared with frontal subregions previously implicated in late-life mood disturbance.

Memory tests that are in a recall format have almost universally measured accuracy in terms of the number of target items reported by the examinee. However, this traditional scoring method can, in certain cases, result in artificially inflated memory accuracy scores. That is, just as a “yes” response bias and high false-positive rate on recognition testing can artificially inflate a patient's hit rate, so, too, a liberal response bias and high intrusion rate on recall testing can artificially inflate a patient's level of target recall. Recognition tests correct for this problem by using a discriminability measure that provides a single score of hit rate relative to false-positive rate; however, recall tests rarely provide a single score of recall accuracy that corrects for intrusion rate. In the present study, we examined the utility of a new recall discriminability measure that analyzes target recall relative to intrusion rate. Patients with Alzheimer's disease (AD) or Huntington's disease (HD) were administered the CVLT–II, which provides both the traditional measure of target recall and a new measure of recall discriminability. The results indicate that the new recall discriminability measure was superior to the traditional level of target recall measure in distinguishing the recall performance of AD and HD patients. Implications of these results for clinical practice and theories of memory disorder in dementia are discussed. (JINS, 2005, 11, 708–715.)

Nearly 3,000,000 people in the United States, and over 100,000,000 people worldwide, are infected with hepatitis C virus (HCV), with an increasing trajectory for the foreseeable future (Alter et al., 1999). While hepatic encephalopathy has been long recognized as a disorder associated with cerebral structural, metabolic, and cognitive changes (e.g., Tarter et al., 1989), HCV infection itself is increasingly associated with changes in the brain, even in the absence of hyperammonemia. Specifically, HCV-infected individuals may have deficits in cognitive functions such as attention, working memory, and speed of information processing (Forton et al., 2002; Hilsabeck et al., 2002). They may also have abnormalities on magnetic resonance spectroscopy (MRS), a non-invasive method to measure cerebral metabolites. The most reliably measured compounds using a standard 1.5 Tesla MRI scanner are N-acetylaspartate (NAA), a marker of neuronal integrity; choline and choline-containing compounds (Cho), a measure of cell membrane turnover and lipid changes; myo-Inositol (Ins), a possible indicator of glial proliferation and/or osmolar changes; and creatine+phosphocreatine (Cr), an indicator of high energy stores that is often used as a relative standard for other metabolites. In the first studies of HCV using MRS, Forton et al. (2001; 2002) found elevated Cho/Cr in the frontal white matter and basal ganglia in patients with HCV. In addition patients with two or more impaired neuropsychological test performances had higher Cho/Cr compared to those with less than two impaired test performances.