ArticleJournal of neurochemistry2012
Ketone bodies protection against HIV-1 Tat-induced neurotoxicity.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- HIV Tat Expression and Cocaine Exposure Lead to Sex- and Age-Specific Changes of the Microbiota Composition in the Gut.Microorganisms · 2023Article
- Neuropathogenesis of HIV and emerging therapeutic targets.Expert opinion on therapeutic targets · 2022Review
- Antiretroviral Drugs Promote Amyloidogenesis by De-Acidifying Endolysosomes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- HIV-1 Tat-Induced Astrocytic Extracellular Vesicle miR-7 Impairs Synaptic Architecture.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Article
- Conditional expression of HIV-1 tat in the mouse alters the onset and progression of tonic, inflammatory and neuropathic hypersensitivity in a sex-dependent manner.European journal of pain (London, England) · 2020Article
- Bioenergetic adaptations to HIV infection. Could modulation of energy substrate utilization improve brain health in people living with HIV-1?Experimental neurology · 2020Review
- MicroRNAs in central nervous system diseases: A prospective role in regulating blood-brain barrier integrity.Experimental neurology · 2020Review
- Role of Endolysosomes in Severe Acute Respiratory Syndrome Coronavirus-2 Infection and Coronavirus Disease 2019 Pathogenesis: Implications for Potential Treatments.Frontiers in pharmacology · 2020Article
- Astrocyte activation and altered metabolism in normal aging, age-related CNS diseases, and HAND.Journal of neurovirology · 2019Review
- HIV-1 infection alters energy metabolism in the brain: Contributions to HIV-associated neurocognitive disorders.Progress in neurobiology · 2019Review
- BK channels regulate extracellular Tat-mediated HIV-1 LTR transactivation.Scientific reports · 2019Article
- Scaling Synapses in the Presence of HIV.Neurochemical research · 2019Review
- Article
- DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Ketone-Based Metabolic Therapy: Is Increased NADFrontiers in molecular neuroscience · 2017Article
- 5α-reduced progestogens ameliorate mood-related behavioral pathology, neurotoxicity, and microgliosis associated with exposure to HIV-1 Tat.Brain, behavior, and immunity · 2016Article
- Release of calcium from endolysosomes increases calcium influx through N-type calcium channels: Evidence for acidic store-operated calcium entry in neurons.Cell calcium · 2015Article
- MSM ameliorates HIV-1 Tat induced neuronal oxidative stress via rebalance of the glutathione cycle.American journal of translational research · 2015Article
- Atg7 deficiency impairs host defense against Klebsiella pneumoniae by impacting bacterial clearance, survival and inflammatory responses in mice.American journal of physiology. Lung cellular and molecular physiology · 2014Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
HIV-1-associated neurocognitive disorder (HAND) is a syndrome that ranges clinically from subtle neuropsychological impairments to profoundly disabling HIV-associated dementia. Not only is the pathogenesis of HAND unclear, but also effective treatments are unavailable. The HIV-1 transactivator of transcription protein (HIV-1 Tat) is strongly implicated in the pathogenesis of HAND, in part, because of its well-characterized ability to directly excite neurons and cause neurotoxicity. Consistent with previous findings from others, we demonstrate here that HIV-1 Tat induced neurotoxicity, increased intracellular calcium, and disrupted a variety of mitochondria functions, such as reducing mitochondrial membrane potential, increasing levels of reactive oxygen species, and decreasing bioenergetic efficiency. Of therapeutic importance, we show that treatment of cultured neurons with ketone bodies normalized HIV-1 Tat induced changes in levels of intracellular calcium, mitochondrial function, and neuronal cell death. Ketone bodies are normally produced in the body and serve as alternative energy substrates in tissues including brain and can cross the blood-brain barrier. Ketogenic strategies have been used clinically for treatment of neurological disorders and our current results suggest that similar strategies may also provide clinical benefits in the treatment of HAND.
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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.