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Open AccessJournal ArticleDOI

HIV-1 associated dementia: symptoms and causes

TLDR
HIV-associated cognitive impairment correlates with the increased presence in the CNS of activated, though not necessarily HIV-1-infected, microglia and CNS macrophages, suggesting that indirect mechanisms of neuronal injury and loss/death occur in HIV/AIDS as a basis for dementia since neurons are not themselves productively infected by HIV- 1.
Abstract
Despite the use of highly active antiretroviral therapy (HAART), neuronal cell death remains a problem that is frequently found in the brains of HIV-1-infected patients. HAART has successfully prevented many of the former end-stage complications of AIDS, however, with increased survival times, the prevalence of minor HIV-1 associated cognitive impairment appears to be rising among AIDS patients. Further, HIV-1 associated dementia (HAD) is still prevalent in treated patients as well as attenuated forms of HAD and CNS opportunistic disorders. HIV-associated cognitive impairment correlates with the increased presence in the CNS of activated, though not necessarily HIV-1-infected, microglia and CNS macrophages. This suggests that indirect mechanisms of neuronal injury and loss/death occur in HIV/AIDS as a basis for dementia since neurons are not themselves productively infected by HIV-1. In this review, we discussed the symptoms and causes leading to HAD. Outcome from this review will provide new information regarding mechanisms of neuronal loss in AIDS patients.

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Microglia: gatekeepers of central nervous system immunology

TL;DR: This review about microglia aims to introduce the reader extensively into their ontogeny, cell biology, and involvement in different neuropathologies.
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Nanolipidic particles improve the bioavailability and α-secretase inducing ability of epigallocatechin-3-gallate (EGCG) for the treatment of Alzheimer's disease

TL;DR: It is found that forming nanolipidic EGCG particles improves the neuronal (SweAPP N2a cells) alpha-secretase enhancing ability in vitro by up to 91% (P<001) and it's oral bioavailability in vivo by more than two-fold over free E GCG.
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The ins and outs of HIV-1 Tat.

TL;DR: Accumulating evidence suggests that extracellular Tat acts as a viral toxin that affects the biological activity of different cell types and has a key role in acquired immune‐deficiency syndrome development.
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Nanotechnology applications for improved delivery of antiretroviral drugs to the brain

TL;DR: By delivering ARVs with nanocarriers, significant increase in the drug bioavailability to the brain is expected to be achieved and future research should focus on achieving brain delivery of ARVs in a safe, efficient, and yet cost-effective manner.
Journal ArticleDOI

HIV-tat induces formation of an LRP–PSD-95– NMDAR–nNOS complex that promotes apoptosis in neurons and astrocytes

TL;DR: The HIV-encoded protein tat triggers formation of a macromolecular complex involving the low-density lipoprotein receptor-related protein (LRP), postsynaptic density protein-95, N-methyl-d-aspartic acid (NMDA) receptors, and neuronal nitric oxide synthase at the neuronal plasma membrane, and this complex leads to apoptosis in neurons negative as well as positive for NMDA receptors and also in astrocytes.
References
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Journal ArticleDOI

Cellular localization of human immunodeficiency virus infection within the brains of acquired immune deficiency syndrome patients

TL;DR: The brains of 12 AIDS patients were studied using in situ hybridization to identify human immunodeficiency virus nucleic acid sequences and immunocytochemistry to identify viral and cellular proteins, suggesting that CNS dysfunction is due to indirect effects rather than neuronal or glial infection.
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Pathways to neuronal injury and apoptosis in HIV-associated dementia

TL;DR: Human immunodeficiency virus-1 (HIV-1) can induce dementia with alarming occurrence worldwide, but discovery in brain of HIV-1-binding sites (chemokine receptors) provides new insights.
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The neuropathogenesis of AIDS

TL;DR: The studies that are being carried out to determine the respective contributions of infection, and monocyte and macrophage activation, to disease progression are discussed.
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Chemokines regulate hippocampal neuronal signaling and gp120 neurotoxicity

TL;DR: Fura-2-based Ca imaging showed that numerous chemokines, including SDF-1alpha, RANTES, and fractalkine, affect neuronal Ca signaling, suggesting that hippocampal neurons possess a wide variety of chemokine receptors.
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Neurodegenerative diseases: a decade of discoveries paves the way for therapeutic breakthroughs.

TL;DR: Understanding of mechanisms regulating protein processing and aggregation, as well as of the toxic effects of misfolded neurodegenerative disease proteins, will facilitate development of rationally designed therapies to treat and prevent these disorders.
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