Aging and Apolipoprotein E in HIV Infection

Geffin, Rebeca; McCarthy, Micheline

doi:10.1007/s13365-018-0660-2

Cited by 19 publications

(20 citation statements)

References 132 publications

(169 reference statements)

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“…Lastly, an interesting set of studies tried to investigate a link between APOE and the modulation of HIV infection as a chronic disease, now that the affected individuals can live to older ages thanks to anti-retroviral therapy. Even though the overall results are somewhat contrasting, isoform ε4 seems to correlate in different cases with the development of HIV-associated neurocognitive disorders, impaired cognition, dyslipidaemia, premature brain aging, and increased chance of debilitating opportunistic infections [116,117,118,119,120] (see also a comprehensive review in Reference [121]).…”

Section: Apoe Function and Pathologymentioning

confidence: 99%

The Genetic Variability of APOE in Different Human Populations and Its Implications for Longevity

Abondio

Sazzini

Garagnani

et al. 2019

Genes

102

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Human longevity is a complex phenotype resulting from the combinations of context-dependent gene-environment interactions that require analysis as a dynamic process in a cohesive ecological and evolutionary framework. Genome-wide association (GWAS) and whole-genome sequencing (WGS) studies on centenarians pointed toward the inclusion of the apolipoprotein E (APOE) polymorphisms ε2 and ε4, as implicated in the attainment of extreme longevity, which refers to their effect in age-related Alzheimer’s disease (AD) and cardiovascular disease (CVD). In this case, the available literature on APOE and its involvement in longevity is described according to an anthropological and population genetics perspective. This aims to highlight the evolutionary history of this gene, how its participation in several biological pathways relates to human longevity, and which evolutionary dynamics may have shaped the distribution of APOE haplotypes across the globe. Its potential adaptive role will be described along with implications for the study of longevity in different human groups. This review also presents an updated overview of the worldwide distribution of APOE alleles based on modern day data from public databases and ancient DNA samples retrieved from literature in the attempt to understand the spatial and temporal frame in which present-day patterns of APOE variation evolved.

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Section: Apoe Function and Pathologymentioning

confidence: 99%

The Genetic Variability of APOE in Different Human Populations and Its Implications for Longevity

Abondio

Sazzini

Garagnani

et al. 2019

Genes

102

View full text Add to dashboard Cite

show abstract

“…HIV-infection accelerates and accentuates premature aging of the nervous system by potentiating, at least in part, immunological senescence, measured by the accumulation of CD28 − /CD57 + T cells [ 78 , 144 ] and activation of the monocyte markers CD163 and CXCL10 [ 145 ]. The neurocognitive performance of young (≤40 years of age) HIV+ patients was found to be equivalent to those of older (≥50 years of age) seronegative individuals [ 146 , 147 ].…”

Section: Contribution Of Host Genes In Alzheimer’s Disease (Ad) Amentioning

confidence: 99%

“…Sections of temporal lobe/hippocampus, entorhinal cortex and frontal lobes from the brains of HIV-1 infected patients obtained at autopsy were immunohistochemically stained with antibodies against Aβ and phosphorylated-tau (p-tau) [ 149 , 153 ]. In contrast to the neuritic Aβ plaques observed in the AD brain, diffusely distributed Aβ plaques and sparsely-scattered neurofibrillary lesions were detected in both HIV cases and non-HIV controls [ 144 ]. Those features correlated with aging rather than symptomatic AD.…”

Section: Contribution Of Host Genes In Alzheimer’s Disease (Ad) Amentioning

confidence: 99%

Risk Factors and Pathogenesis of HIV-Associated Neurocognitive Disorder: The Role of Host Genetics

Olivier

Cacabelos

Naidoo

2018

IJMS

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Neurocognitive impairments associated with human immunodeficiency virus (HIV) infection remain a considerable health issue for almost half the people living with HIV, despite progress in HIV treatment through combination antiretroviral therapy (cART). The pathogenesis and risk factors of HIV-associated neurocognitive disorder (HAND) are still incompletely understood. This is partly due to the complexity of HAND diagnostics, as phenotypes present with high variability and change over time. Our current understanding is that HIV enters the central nervous system (CNS) during infection, persisting and replicating in resident immune and supporting cells, with the subsequent host immune response and inflammation likely adding to the development of HAND. Differences in host (human) genetics determine, in part, the effectiveness of the immune response and other factors that increase the vulnerability to HAND. This review describes findings from studies investigating the role of human host genetics in the pathogenesis of HAND, including potential risk factors for developing HAND. The similarities and differences between HAND and Alzheimer’s disease are also discussed. While some specific variations in host genes regulating immune responses and neurotransmission have been associated with protection or risk of HAND development, the effects are generally small and findings poorly replicated. Nevertheless, a few specific gene variants appear to affect the risk for developing HAND and aid our understanding of HAND pathogenesis.

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“…Genetic variation in human apoprotein E (ApoE) has been identified as a possible risk factor for developing HAND, although this is still a subject of debate (Geffin and McCarthy 2018). The ApoE gene encodes a 34 kDa protein involved in transport and metabolism of both triglyceride and cholesterol (Bellosta et al 1995;Mannila et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Childhood trauma interacts with ApoE to influence neurocognitive function in women living with HIV

et al. 2018

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HIV-associated neurocognitive disorder (HAND) describes a spectrum of behavioural, motor and cognitive disturbances that can occur secondary to HIV infection. Less severe forms of the disorder persist despite advances in antiretroviral medication efficacy and availability. Childhood trauma (CT) may predispose individuals to developing HAND. As genetic variation in human apolipoprotein E (ApoE) has been implicated in cognitive decline and may mediate the development of long-term health outcomes following CT, we investigated the influence of ApoE and CT on cognitive function in the context of HIV. One hundred twenty-eight HIV-positive Xhosa women completed the Childhood Trauma Questionnaire-Short Form (CTQ-SF) as well as the HIV Neurobehavioral Research Center neurocognitive test battery. rs7412 and rs429358 were genotyped using KASP assays, and this data was used to determine the ApoE isoform. Baseline differences in demographic and clinical variables according to CT exposure were calculated. Analysis of covariance was used to assess the contributions of CT and ApoE variants, as well as their interaction, to cognitive function. Eighty-eight participants reported experiencing CT. The rs7412 C allele protected against the harmful effect of CT on motor scores using an additive model. The interaction of ApoE ε4 and CT was associated with worse attention/working memory scores. ApoE ε4, alone and in combination with CT, is associated with poorer cognitive function. Further research into this gene-environment interaction may assist in identifying at-risk individuals for targeted interventions.

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Aging and Apolipoprotein E in HIV Infection

Cited by 19 publications

References 132 publications

The Genetic Variability of APOE in Different Human Populations and Its Implications for Longevity

The Genetic Variability of APOE in Different Human Populations and Its Implications for Longevity

Risk Factors and Pathogenesis of HIV-Associated Neurocognitive Disorder: The Role of Host Genetics

Childhood trauma interacts with ApoE to influence neurocognitive function in women living with HIV

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