Evidence map›Paper›PMID 31016584›Full record

ReviewJournal of neurovirology2019

HIV and Alzheimer's disease: complex interactions of HIV-Tat with amyloid β peptide and Tau protein.

Alina Hategan, Eliezer Masliah, Avindra Nath

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neurovirology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 47 citations in OpenAlex.

  1. Increased Amyloidogenic Neuronal Injury in HIV-1-infected APP-KI Alzheimer's disease mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Alina HateganSection of Infections of the Nervous System, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bldg 10; Room 7C-103, 10 Center Drive, Bethesda, MD, 20892, USA.
Eliezer MasliahDivision of Neuroscience, National Institute of Aging, National Institutes of Health, 7201 Wisconsin Ave, Bethesda, MD, 20892, USA.
Avindra NathSection of Infections of the Nervous System, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bldg 10; Room 7C-103, 10 Center Drive, Bethesda, MD, 20892, USA. natha@ninds.nih.gov.ORCID 0000-0003-0927-5855
National Institutes of Health · US

Funding

Neuropathogenesis of Retroviral InfectionsZIANS003130 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI NATH, AVINDRA · 2011 to 2025
$73.7M
Neuroimmune responses and therapeutics of alpha-synucleinopathies of the aging populationZIAAG000936 · NIA · NATIONAL INSTITUTE ON AGING · PI COOKSON, MARK · 2017 to 2025
$4.1M
Intramural NIH HHS ZIA NS003130National Institute of Neurological Disorders and Stroke (US) NS003130
6 · The paper itself

Abstract

In patients infected with the human immunodeficiency virus (HIV), the HIV-Tat protein may be continually produced despite adequate antiretroviral therapy. As the HIV-infected population is aging, it is becoming increasingly important to understand how HIV-Tat may interact with proteins such as amyloid β and Tau which accumulate in the aging brain and eventually result in Alzheimer's disease. In this review, we examine the in vivo data from HIV-infected patients and animal models and the in vitro experiments that show how protein complexes between HIV-Tat and amyloid β occur through novel protein-protein interactions and how HIV-Tat may influence the pathways for amyloid β production, degradation, phagocytosis, and transport. HIV-Tat may also induce Tau phosphorylation through a cascade of cellular processes that lead to the formation of neurofibrillary tangles, another hallmark of Alzheimer's disease. We also identify gaps in knowledge and future directions for research. Available evidence suggests that HIV-Tat may accelerate Alzheimer-like pathology in patients with HIV infection which cannot be impacted by current antiretroviral therapy.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnti-HIV AgentsBrain ChemistryExtracellular SpaceHIV InfectionsHumansLow Density Lipoprotein Receptor-Related Protein-1LysosomesMacrophagesMiceModels, MolecularNeprilysinNeurofibrillary TanglesNeurogliaAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Anti-HIV AgentsLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanMAPT protein, humanNeprilysinPeptide Fragmentstat Gene Products, Human Immunodeficiency Virustau ProteinsAggregationAIDSAlzheimer’s diseaseBrainDementiaHIV-TatNeurodegenerationProtein misfolding

Identifiers

PMID31016584
PMCPMC9056081
OpenAlexW2940958170

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.