ArticleFrontiers in microbiology2015
HIV-1 Tat and cocaine mediated synaptopathy in cortical and midbrain neurons is prevented by the isoflavone Equol.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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.
Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- S-Equol: a novel therapeutic for HIV-1-associated gastrointestinal dysbiosis.NeuroImmune pharmacology and therapeutics · 2025Article
- Estrogen Modulation of B Cell Immunity: Implications for HIV Control and Therapeutic Strategies.Comprehensive physiology · 2025Review
- Equol as a Multitarget Agent Against Neurodegeneration: Mechanistic Insights into Its Molecular Modulation.Neuromolecular medicine · 2025Review
- Suppression of HIV-TAT and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters.Journal of neurovirology · 2024Article
- Suppression of HIV and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters.bioRxiv : the preprint server for biology · 2023Article
- Therapeutically targeting the consequences of HIV-1-associated gastrointestinal dysbiosis: Implications for neurocognitive and affective alterations.Pharmacology, biochemistry, and behavior · 2023Article
- Astrocytes: Role in pathogenesis and effect of commonly misused drugs in the HIV infected brain.Current research in neurobiology · 2023Review
- The Epigenetic Role of miR-124 in HIV-1 Tat- and Cocaine-Mediated Microglial Activation.International journal of molecular sciences · 2022Article
- Review
- Allopregnanolone and neuroHIV: Potential benefits of neuroendocrine modulation in the era of antiretroviral therapy.Journal of neuroendocrinology · 2022Review
- S-Equol mitigates motivational deficits and dysregulation associated with HIV-1.Scientific reports · 2021Article
- HIV-1 Tat promotes age-related cognitive, anxiety-like, and antinociceptive impairments in female mice that are moderated by aging and endocrine status.GeroScience · 2021Article
- S-EQUOL: a neuroprotective therapeutic for chronic neurocognitive impairments in pediatric HIV.Journal of neurovirology · 2020Article
- Inflammation-induced PINCH expression leads to actin depolymerization and mitochondrial mislocalization in neurons.Translational neurodegeneration · 2020Article
- Selective Estrogen Receptor β Agonists: a Therapeutic Approach for HIV-1 Associated Neurocognitive Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Article
- Combined HIV-1 Tat and oxycodone activate the hypothalamic-pituitary-adrenal and -gonadal axes and promote psychomotor, affective, and cognitive dysfunction in female mice.Hormones and behavior · 2020Article
- A Novel Mechanism of S-equol Action in Neurons and Astrocytes: The Possible Involvement of GPR30/GPER1.International journal of molecular sciences · 2019Article
- Neurorestoration of Sustained Attention in a Model of HIV-1 Associated Neurocognitive Disorders.Frontiers in behavioral neuroscience · 2019Article
- The role of G-protein-coupled membrane estrogen receptor in mouse Leydig cell function-in vivo and in vitro evaluation.Cell and tissue research · 2018Article
- HIV-1 proteins dysregulate motivational processes and dopamine circuitry.Scientific reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Illicit drugs, such as cocaine, are known to increase the likelihood and severity of HIV-1 associated neurocognitive disorders (HAND). In the current studies synaptic integrity was assessed following exposure to low concentrations of the HIV-1 viral protein Tat 1-86B, with or without cocaine, by quantifying filamentous actin (F-actin) rich structures (i.e., puncta and dendritic spines) on neuronal dendrites in vitro. In addition, the synapse-protective effects of either R-Equol (RE) or S-Equol (SE; derivatives of the soy isoflavone, daidzein) were determined. Individually, neither low concentrations of HIV-1 Tat (10 nM) nor low concentrations of cocaine (1.6 μM) had any significant effect on F-actin puncta number; however, the same low concentrations of HIV-1 Tat + cocaine in combination significantly reduced dendritic synapses. This synaptic reduction was prevented by pre-treatment with either RE or SE, in an estrogen receptor beta dependent manner. In sum, targeted therapeutic intervention with SE may prevent HIV-1 + drug abuse synaptopathy, and thereby potentially influence the development of HAND.
Indexed as
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.