Prevalence of cognitive disorders differs as a function of age in HIV virus infection. AIDS

Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
AIDS (Impact Factor: 6.56). 02/2004; 18 Suppl 1(Supplement 1):S11-8. DOI: 10.1097/00002030-200401001-00003
Source: PubMed

ABSTRACT Ten per cent of all new cases of AIDS in the United States are in persons older than 50 years. This is particularly problematical in the case of the neuropsychiatric consequences of HIV, because there are neuropsychiatric disorders which become common in older individuals in the absence of HIV. The purpose of this report is to describe the prevalence and incidence of cognitive impairment in HIV-infected individuals enrolled in a community-based study.
The study consisted of community-based, sentinel survey physician referrals of HIV-infected patients, with volunteer recruitment of risk-appropriate seronegative controls. One-year longitudinal follow-up study.
Detailed neuropsychiatric evaluations were performed at study entry and after one year. A brief, interim visit tracked incident change. Each subject's neuropsychological test performance was classified as normal, demented, or cognitive impairment (not demented).
The prevalence of cognitive disorder among HIV-positive individuals over 50 years was significantly greater than in individuals younger than 50 years. Among older participants, dementia was the more common classification (23%), whereas among younger participants, a milder form of cognitive impairment was more prevalent (22%). Alcohol abuse/dependence was a significant risk factor for a disorder, whereas greater education was a protective factor. The one-year incidence of disorder in the sample overall was low (7.3%), and age was not a significant risk factor. However, HIV viral load at study entry was significantly higher among those participants who had developed cognitive impairment one year later.
Age is a significant risk modifier for prevalent neuropsychological disorder.

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    • "In fact, studies have shown that even after 1 year of being diagnosed with HIV, changes in brain chemistry and metabolism are evident which correspond to poorer cognitive performance [28] [29] [30]. Given that increasing age is associated with more cognitive complaints, cognitive deficits, and the risk for pathological cognitive aging (i.e., Alzheimer's disease, vascular dementia, and Lewy body dementia) [31] [32] [33], concerns mount that as people age with HIV, they may become more vulnerable for developing such cognitive deficits and dementia (Figure 1; [34] [35] [36] [37] [38]). As highlighted in Figure 1, this risk is further increased since HIV produces systemic inflammation and neuroinflammation which may accelerate normal aging and brain aging, respectively [39] [40] [41] [42]. "
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    ABSTRACT: Highly active antiretroviral therapy has given the chance to those living with HIV to keep on living, allowing them the opportunity to age and perhaps age successfully. Yet, there are severe challenges to successful aging with HIV, one of which is cognitive deficits. Nearly half of those with HIV experience cognitive deficits that can interfere with everyday functioning, medical decision making, and quality of life. Given that cognitive deficits develop with more frequency and intensity with increasing age, concerns mount that as people age with HIV, they may experience more severe cognitive deficits. These concerns become especially germane given that by 2015, 50% of those with HIV will be 50 and older, and this older cohort of adults is expected to grow. As such, this paper focuses on the etiologies of such cognitive deficits within the context of cognitive reserve and neuroplasticity. From this, evidence-based and hypothetical prevention (i.e., cognitive prescriptions), rehabilitation (i.e., speed of processing training), and mitigation (i.e., spaced retrieval method) strategies are reviewed. Implications for nursing practice and research are posited.
    02/2013; 2013:297173. DOI:10.1155/2013/297173
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    • "Searching for the mechanisms of HAND neuropathogenesis, and identifying early indicators and biomarkers of HAND, are central themes of neuroAIDS research. Currently, several factors are useful for identifying individuals who are inherently or chronically at risk for HAND, including demographic characteristics [Becker et al., 2004; Cherner et al., 2004; Valcour et al., 2004b], medical comorbidities [Qureshi et al., 1998; Cherner et al., 2005; Tozzi et al., 2005; Valcour et al., 2005; Lin et al., 2011], and lifestyle behaviors, in particular substance abuse [Rippeth et al., 2004; Levine et al., 2006; Martin-Thormeyer and Paul, 2009]. In addition, host genetic factors have received attention, both as a means to identify risk factors and to determine the neuropathogenesis of HAND. "
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    ABSTRACT: The neuropathogenesis of HIV-associated neurocognitive disorders (HAND) is unclear. Candidate gene studies have implicated genetic susceptibility loci within immune-related genes; however, these have not been reliably validated. Here, we employed genome-wide association (GWA) methods to discover novel genetic susceptibility loci associated with HAND, and validate susceptibility loci implicated in prior candidate gene studies. Data from 1,287 participants enrolled in the Multicenter AIDS Cohort Study between 1985 and 2010 were used. Genotyping was conducted with Illumina 1M, 1MDuo, or 550K platform. Linear mixed models determined subject-specific slopes for change over time in processing speed and executive functioning, considering all visits including baseline and the most recent study visit. Covariates modeled as fixed effects included: time since the first visit, depression severity, nadir CD4+ T-cell count, hepatitis C co-infection, substance use, and antiretroviral medication regimen. Prevalence of HIV-associated dementia (HAD) and neurocognitive impairment (NCI) was also examined as neurocognitive phenotypes in a case-control analysis. No genetic susceptibility loci were associated with decline in processing speed or executive functioning among almost 2.5 million single nucleotide polymorphisms (SNPs) directly genotyped or imputed. No association between the SNPs and HAD or NCI were found. Previously reported associations between specific genetic susceptibility loci, HIV-associated NCI, and HAD were not validated. In this first GWAS of HAND, no novel or previously identified genetic susceptibility loci were associated with any of the phenotypes examined. Due to the relatively small sample size, future collaborative efforts that incorporate this dataset may still yield important findings.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 09/2012; 159B(6):669-83. DOI:10.1002/ajmg.b.32071 · 3.27 Impact Factor
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    • "However, conflicting findings are noted in other studies and, if evidence for deficits is present, the age at which these findings would translate into clinically relevant outcomes remains to be defined. Becker et al. reported higher rates of neuropsychological testing abnormalities among older compared to younger individuals in the Allegheny County Neuropsychological Survey (Becker et al. 2004). This study included 290 HIV+ and 114 HIV-negative individuals. "
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    ABSTRACT: Cognitive efficiency decreases with age, and advancing age is the leading risk factor for most neurodegenerative disorders that result in dementia. In HIV infection, risk for cognitive impairment is consistently linked to advancing chronological age. As the HIV epidemic enters its fourth decade in the USA, extended life expectancy will likely result in an increased prevalence of cognitive disorders by virtue of these factors. However, it is less clear if HIV potentiates or accelerates the risk for cognitive impairment given that most reports are mixed or demonstrate only a small interaction effect. More critically, it is unclear if HIV will modulate the neuropathology associated with non-HIV cognitive disorders in a manner that will increase risk for diseases such as cerebrovascular and Alzheimer's disease. In the coming years, with increasing numbers of HIV+ patients entering their 60s and 70s, background risk for neurodegenerative disorders will be sufficiently high as to inform this issue on clinical grounds. This review summarizes knowledge of cognition in HIV as it relates to age and presents some emerging controversies.
    Journal of NeuroVirology 04/2012; 18(4):256-63. DOI:10.1007/s13365-012-0094-1 · 3.32 Impact Factor
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