ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2007
Glycogen synthase kinase 3 beta (GSK-3 beta) as a therapeutic target in neuroAIDS.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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
33 citing papers in PubMed, 42 citations in OpenAlex.
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- Discovery of Dual Targeting GSK-3β/HIV-1 Reverse Transcriptase Inhibitors as Neuroprotective Antiviral Agents.ACS chemical neuroscience · 2025Article
- Identification of Novel GSK-3β Hits Using Competitive Biophysical Assays.International journal of molecular sciences · 2022Article
- Glycogen synthase kinase (GSK)-3 and the double-strand RNA-dependent kinase, PKR: When two kinases for the common good turn bad.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Rosmarinic Acid Derivatives' Inhibition of Glycogen Synthase Kinase-3β Is the Pharmacological Basis of Kangen-Karyu in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2018Article
- The role of human dopamine transporter in NeuroAIDS.Pharmacology & therapeutics · 2018Review
- Mass spectrometric phosphoproteome analysis of HIV-infected brain reveals novel phosphorylation sites and differential phosphorylation patterns.Proteomics. Clinical applications · 2016Article
- Glycogen Synthase Kinase-3 (GSK-3)-Targeted Therapy and Imaging.Theranostics · 2016Review
- HIV-1-Tat Protein Inhibits SC35-mediated Tau Exon 10 Inclusion through Up-regulation of DYRK1A Kinase.The Journal of biological chemistry · 2015Article
- Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases.Pharmacology & therapeutics · 2015Review
- GSK3β-activation is a point of convergence for HIV-1 and opiate-mediated interactive neurotoxicity.Molecular and cellular neurosciences · 2015Article
- Mechanisms of HIV-1 Tat neurotoxicity via CDK5 translocation and hyper-activation: role in HIV-associated neurocognitive disorders.Current HIV research · 2015Review
- Neuroprotective effects of the anti-cancer drug sunitinib in models of HIV neurotoxicity suggests potential for the treatment of neurodegenerative disorders.British journal of pharmacology · 2014Article
- Adjunctive and long-acting nanoformulated antiretroviral therapies for HIV-associated neurocognitive disorders.Current opinion in HIV and AIDS · 2014Review
- The role of tau protein in HIV-associated neurocognitive disorders.Molecular neurodegeneration · 2014Review
- Glycogen synthase kinase-3 inhibitors: Rescuers of cognitive impairments.Pharmacology & therapeutics · 2014Review
- Improving lithium therapeutics by crystal engineering of novel ionic cocrystals.Molecular pharmaceutics · 2013Article
- Targeting platelet-derived soluble CD40 ligand: a new treatment strategy for HIV-associated neuroinflammation?Journal of neuroinflammation · 2013Review
- Discovery, synthesis, and characterization of an orally bioavailable, brain penetrant inhibitor of mixed lineage kinase 3.Journal of medicinal chemistry · 2013Article
- Autophagy in dementias.Brain pathology (Zurich, Switzerland) · 2012Review
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 3 institutions in 1 country.
Funding
Abstract
Highly active antiretroviral therapy (HAART) has made a significant impact on the lives of people living with HIV-1 infection. The incidence of neurologic disease associated with HIV-1 infection of the CNS plummeted between 1996-2000, but unfortunately the number of people currently HIV-1 infected (i.e., prevalence) with associated cognitive impairment has been steadily rising. While the reasons for this may be multifactorial, the implication is clear: there is a pressing need for adjunctive therapy directed at reversing or preventing damage to vulnerable pathways in the central nervous system (CNS) from HIV-1 infection. Using a team of preclinical and clinical investigators, we have focused our efforts on defining how proinflammatory mediators and secretory neurotoxins from HIV-1 disrupt signaling of the survival-regulating enzyme, glycogen synthase kinase 3 beta (GSK-3beta). In a series of studies initiated using in vitro, then in vivo models of HIV-1-associated dementia (HAD), we have demonstrated the ability of the mood stabilizing and anticonvulsant drug, sodium valproate (VPA), that inhibits GSK-3beta activity and other downstream mediators, to reverse HIV-1-induced damage to synaptic pathways in the CNS. Based on these results, we successfully performed pharmacokinetic and safety and tolerability trials with VPA in a cohort of HIV-1-infected patients with neurologic disease. VPA was well tolerated in this population and secondary measures of brain metabolism, as evidenced by an increase in N-acetyl aspartate/creatine (NAA/Cr), further suggested that VPA may improve gray matter integrity in brain regions damaged by HIV-1. These findings highlight the therapeutic potential of GSK-3beta blockade.
Indexed as
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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.