ArticleClinical research in HIV/AIDS2014
Amyloid beta accumulation in HIV-1 infected brain: the role of altered cholesterol homeostasis.
Article in Clinical research in HIV/AIDS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Human immunodeficiency virus 1 glycoprotein 120 induces endoplasmic reticulum stress in neurons.Cell death & disease · 2025Article
- Article
- Complement component 3 and complement factor H protein levels are altered in brain tissues from people with human immunodeficiency virus: A pilot study.Frontiers in aging neuroscience · 2022Article
- Microwave & magnetic proteomics of macrophages from patients with HIV-associated cognitive impairment.PloS one · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The long-term survival of HIV-1 infected individuals credited to the availability and use of effective antiretroviral therapy (ART) is unfortunately now accompanied by an almost 50% prevalence of HIV-1 associated neurocognitive disorder (HAND). Increasingly, it has been realized that HIV-1 infected people on ART have clinical and pathological observations of Alzheimer's disease (AD)-like manifestations including neurocognitive problems, intraneuronal accumulation of amyloid beta (Aβ) protein, and disturbed synaptic integrity. Part of the current challenge facing the medical community and people living with HIV-1 infection is that the pathogenesis of HAND remains unclear, and little is known about how AD-like pathology is developed as a result of HIV-1 infection and/or long-term ART treatment. Here we discuss the potential role of altered plasma cholesterol homeostasis, a prominent feature of HIV-1 infection, on the development of intraneuronal Aβ accumulation in HIV-1 infected brain. We speculate that elevated plasma LDL cholesterol, once it enters brain parenchyma via an increasingly leaky BBB, can be internalized by neurons via receptor-mediated endocytosis, a process that could promote internalization of amyloid beta precursor protein (AβPP). Unlike brain
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30197929PMC6124677W3021332243What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.