ArticleNature structural & molecular biology2017
HIV Tat protein and amyloid-β peptide form multifibrillar structures that cause neurotoxicity.
Article in Nature structural & molecular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 90 citations in OpenAlex.
- Antiretroviral Therapy Intensification for Neurocognitive Impairment in Human Immunodeficiency Virus.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023Trial
- Blood and cerebrospinal fluid biomarker changes in patients with HIV-associated neurocognitive impairment treated with lithium: analysis from a randomised placebo-controlled trial.Journal of neurovirology · 2023Trial
- Review
- Convergence of neuroinflammation across major neurotropic viral exposomes in AD and ADRD.Journal of neuroinflammation · 2026Review
- Review
- HIF-1 Targeting Intervention Renders Protection From Alzheimer's-Like Pathology in a Humanized Mice Model of HIV Infection.Journal of extracellular vesicles · 2025Article
- Modulation of AβJournal of chemical information and modeling · 2025Article
- Human immunodeficiency virus 1 glycoprotein 120 induces endoplasmic reticulum stress in neurons.Cell death & disease · 2025Article
- Microglial Dysfunction and Amyloid-Beta Pathology in Alzheimer's Disease and HIV-Associated Neurocognitive Disorders.International journal of molecular sciences · 2025Review
- Human Brain Organoids: Development and Applications.Journal of microbiology and biotechnology · 2025Review
- Neurotropic Viruses as Acute and Insidious Drivers of Aging.Biomolecules · 2025Review
- Proteomic Analysis of Chronic Binge Alcohol-Induced Hippocampal and Anterior Cingulate Cortex Neuroadaptations in Simian Immunodeficiency Virus (SIV)-Infected Female Rhesus Macaques.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Viruses and the Brain-A Relationship Prone to Trouble.Viruses · 2025Review
- HIV-1 Vpu induces neurotoxicity by promoting Caspase 3-dependent cleavage of TDP-43.EMBO reports · 2024Article
- Changes in cerebrospinal fluid proteins across the spectrum of untreated and treated chronic HIV-1 infection.PLoS pathogens · 2024Article
- Article
- Neuropathogenic role of astrocyte-derived extracellular vesicles in HIV-associated neurocognitive disorders.Journal of extracellular vesicles · 2024Article
- Viral Infections, Are They a Trigger and Risk Factor of Alzheimer's Disease?Pathogens (Basel, Switzerland) · 2024Review
- Functionalized nanoparticles to deliver nucleic acids to the brain for the treatment of Alzheimer's disease.Frontiers in pharmacology · 2024Review
- The elusive role of herpesviruses in Alzheimer's disease: current evidence and future directions.NeuroImmune pharmacology and therapeutics · 2023Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Deposition of amyloid-β plaques is increased in the brains of HIV-infected individuals, and the HIV transactivator of transcription (Tat) protein affects amyloidogenesis through several indirect mechanisms. Here, we investigated direct interactions between Tat and amyloid-β peptide. Our in vitro studies showed that in the presence of Tat, uniform amyloid fibrils become double twisted fibrils and further form populations of thick unstructured filaments and aggregates. Specifically, Tat binding to the exterior surfaces of the Aβ fibrils increases β-sheet formation and lateral aggregation into thick multifibrillar structures, thus producing fibers with increased rigidity and mechanical resistance. Furthermore, Tat and Aβ aggregates in complex synergistically induced neurotoxicity both in vitro and in animal models. Increased rigidity and mechanical resistance of the amyloid-β-Tat complexes coupled with stronger adhesion due to the presence of Tat in the fibrils may account for increased damage, potentially through pore formation in membranes.
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Identifiers
What 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.