The effects of HIV disease and older age on laboratory-based, naturalistic, and self-perceived symptoms of prospective memory: does retrieval cue type and delay interval matter?

Avci, Gunes; Loft, Shayne; Sheppard, David P.; Woods, Steven Paul

doi:10.1080/13825585.2016.1161001

Cited by 21 publications

(25 citation statements)

References 77 publications

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“…Compared to HIVcontrols, HIV + participants were younger in four studies [43][44][45]50] and older in two studies [29,51]. There were also differences in other demographic factors such as education and ethnicity between HIV + and HIV-participants in 11 studies [40][41][42][43][44][45][50][51][52][53], and they controlled these factors in the analyses.…”

Section: Inclusion Of Hiv-controlsmentioning

confidence: 99%

Is There Any Evidence of Premature, Accentuated and Accelerated Aging Effects on Neurocognition in People Living with HIV? A Systematic Review

et al. 2020

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Despite evidence of premature, accentuated and accelerated aging for some age-related conditions such as cardiovascular diseases in people living with HIV (PLHIV), the evidence for these abnormal patterns of aging on neurocognition remains unclear. Further, no systematic review has been dedicated to this issue. Using PRISMA guidelines, we searched standard databases (PubMed, EMBASE, CINAHL and PsycINFO). Articles were included if they analyzed and reported the effect of age on neurocognition among PLHIV as one of their major findings, if they were conducted in the combination anti-retroviral therapy era (after 1996) and published in a peer-reviewed journal in English. Quality appraisal was conducted using the Joanna Briggs Institute (JBI) appraisal tools. To systematically target the abnormal patterns of neurocognitive aging, we define premature cognitive aging as significant interaction effect of HIV status and age on cross-sectional neurocognitive test performance covering both the normal and abnormal performance range; accentuated cognitive aging as significant interaction effect of HIV status and age on cross-sectional neurocognitive impairment (NCI) rate, thus covering the abnormal performance range only; accelerated cognitive aging as significant interaction effect of HIV status and age on longitudinal neurocognitive test performance or incidence of NCI. Because these definitions require an age-comparable HIV-negative (HIV−) control group, when no controls were included, we determined the range of the age effect on neurocognitive test performance or NCI among PLHIV. A total of 37 studies originating from the US (26), UK (2), Italy (2), Poland (2), China (2), Japan (1), Australia (1), and Brazil (1) were included. Six studies were longitudinal and 14 included HIV- controls. The quality appraisal showed that 12/37 studies neither used an age-matched HIV- controls nor used demographically corrected cognitive scores. A meta-analysis was not possible because study methods and choice of neurocognitive measurement methods and outcomes were heterogeneous imposing a narrative synthesis. In studies with an HIV- control sample, premature neurocognitive aging was found in 45% of the cross-sectional analyses (9/20), while accelerated neurocognitive aging was found in 75% of the longitudinal analyses (3/4). There was no evidence for accentuated aging, but this was tested only in two studies. In studies without an HIV- control sample, the age effect was always present but wide (NCI OR = 1.18–4.8). While large sample size (> 500) was associated with abnormal patterns of cognitive aging, most of the studies were under powered. Other study characteristics such as longitudinal study design and higher proportion of older participants were also associated with the findings of abnormal cognitive aging. There is some support for premature and accelerated cognitive aging among PLHIV in the existing literature especially among large and longitudinal studies and those with higher proportion of older samples. Future HIV and cognitive aging studies need to harmonize neuropsychological measurement methods and outcomes and use a large sample from collaborative multi-sites to generate more robust evidences.

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Section: Inclusion Of Hiv-controlsmentioning

confidence: 99%

Is There Any Evidence of Premature, Accentuated and Accelerated Aging Effects on Neurocognition in People Living with HIV? A Systematic Review

et al. 2020

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“…In that study, younger HIV+ adults’ (mean age, 37.5 years) performance was similar to that of older seronegative adults (mean age, 70 years) on tests of learning, delayed memory, processing speed and attention, visuospatial processing, and language, suggesting that the average 40-year old with HIV had the same cognitive status as a healthy 70-year old. A careful review of more recent cART era studies suggests a similar pattern of accelerated neurocognitive aging (e.g., Woods et al 2010; Avci et al 2016). Across many of these studies, a stair-step effect is observed whereby age and HIV have an additive impact on neurocognitive outcomes.…”

mentioning

confidence: 99%

“…Specifically, younger HIV+ groups reliably perform comparably to older HIV− groups, and both of these groups perform more poorly than older HIV+ groups. For example, several papers show that the memory functioning of HIV+ individuals in their mid-30s are comparable to HIV− individuals in their mid-50s (Avci et al 2016; Woods et al 2010; Scott et al 2011). While most studies have reliably shown differences between HIV+ adults and age-matched seronegative comparison subjects (potentially supporting accentuated aging), no studies in the cART era have directly examined whether older HIV+ adults – who may be at greatest risk to experience both accelerated and accentuated aging – evidence neurocognitive profiles similar to those of much older seronegative adults.…”

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confidence: 99%

Accelerated and accentuated neurocognitive aging in HIV infection

et al. 2017

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There is debate as to whether the neurocognitive changes associated with HIV infection represent an acceleration of the typical aging process or more simply reflect a greater accentuated risk for age-related declines. We aimed to determine whether accelerated neurocognitive aging is observable in a sample of older HIV-infected individuals compared to age-matched seronegatives and older-old (i.e., aged ≥ 65) seronegative adults. Participants in a cross-sectional design included 48 HIV-seronegative (O−) and 40 HIV-positive (O+) participants between the ages of 50–65 (mean ages = 55 and 56, respectively) and 40 HIV-seronegative participants aged ≥ 65 (OO−; mean age = 74) who were comparable for other demographics. All participants were administered a brief neurocognitive battery of attention, episodic memory, speeded executive functions, and confrontation naming (i.e., Boston Naming Test). The O+ group performed more poorly than the O− group (i.e., accentuated aging), but not differently from the OO− on digit span and initial recall of a supraspan word list, consistent with an accelerating aging profile. However, the O+ group’s performance was comparable to the O− group on all other neurocognitive tests (ps > .05). These data partially support a model of accelerated neurocognitive aging in HIV-infection, which was observed in the domain of auditory verbal attention, but not in the areas of memory, language, or speeded executive functions. Future studies should examine whether HIV-infected adults over 65 evidence accelerated aging in downstream neurocognitive domains and subsequent everyday functioning outcomes.

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“…These earlier studies highlighted the need for a carefully matched SN control population in studies where neurocognitive performance may be associated with aging but may also be impacted by other health and lifestyle factors such as alcohol or tobacco use. More recent neuropsychological studies, reported in the current decade, suggest that age and HIV infection have an additive impact on neurocognitive performance, with younger HIV-infected individuals performing comparably to older SN individuals in neurocognitive tests, suggestive of accelerated aging (Avci et al 2016 ; Scott et al 2011 ; Woods et al 2010 ). Sheppard et al ( 2015 ) started with a group of cognitively normal individuals and tested their neurocognitive performance approximately 14 months later.…”

Section: Neurocognitive Changes and Chronic Hiv Infection: Acceleratementioning

confidence: 94%

Aging and Apolipoprotein E in HIV Infection

Geffin

McCarthy

2018

J. Neurovirol.

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With the implementation of increasingly effective antiretroviral therapy (ART) over the past three decades, individuals infected with HIV live a much longer life. HIV infection is no longer a terminal but rather a chronic disease. However, the lifespan of infected individuals remains shorter than that of their uninfected peers. Even with ART, HIV infection may potentiate “premature” aging. Organ-associated disease and systemic syndromes that occur in treated HIV-infection are like that of older, uninfected individuals. Brain aging may manifest as structural changes or neurocognitive impairment that are beyond the chronological age. The spectrum of neurological, cognitive, and motor deficiencies, currently described as HIV-associated neurocognitive disorders (HAND), may reflect earlier onset of mechanisms common to HIV infection and aging (accelerated aging). HAND could also reflect the neurological impact of HIV infection superimposed on comorbidities linked to age and chronic inflammation, leading to a higher prevalence of neurocognitive impairment across the age span (accentuated aging). In addition, apolipoprotein E (ApoE), one of the most influential host risk factors for developing Alzheimer’s disease, has been implicated in the development of HAND. But studies differ as to whether ApoE is relevant, and whether age and ApoE interact to impair brain function in the HIV-infected patient. What is clear is that HIV-infected individuals are living longer with HIV, and therefore factors related to aging and health need to be examined in the context of current, effective ART. This review addresses the recent evidence for the influence of aging and ApoE on HIV-associated neurocognitive impairment.Electronic supplementary materialThe online version of this article (10.1007/s13365-018-0660-2) contains supplementary material, which is available to authorized users.

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The effects of HIV disease and older age on laboratory-based, naturalistic, and self-perceived symptoms of prospective memory: does retrieval cue type and delay interval matter?

Cited by 21 publications

References 77 publications

Is There Any Evidence of Premature, Accentuated and Accelerated Aging Effects on Neurocognition in People Living with HIV? A Systematic Review

Is There Any Evidence of Premature, Accentuated and Accelerated Aging Effects on Neurocognition in People Living with HIV? A Systematic Review

Accelerated and accentuated neurocognitive aging in HIV infection

Aging and Apolipoprotein E in HIV Infection

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