ArticleMolecular neurodegeneration2013
Voluntary exercise protects against methamphetamine-induced oxidative stress in brain microvasculature and disruption of the blood-brain barrier.
Article in Molecular neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 90 citations in OpenAlex.
- Article
- Physical exercise promotes white matter repair after ischemic stroke.Neural regeneration research · 2026Article
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- Aerobic exercise for substance use disorders: therapeutic effects and underlying mechanisms.Frontiers in medicine · 2026Review
- Voluntary wheel exercise reduces pain behavior by modulating neuroinflammation in neuropathic pain.Frontiers in molecular neuroscience · 2026Review
- The impact of endurance training on reducing inflammatory markers in the cardiac tissue of methamphetamine-exposed rats.PloS one · 2026Article
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
- Increase of α-Synuclein in the Peripheral Blood of Subjects with Methamphetamine Use Disorder.Psychiatry investigation · 2025Article
- Circadian misalignment potentiates blood-brain barrier disruption and mitochondria dysregulation in Zika virus infection.Fluids and barriers of the CNS · 2025Article
- The interaction between central and peripheral immune systems in methamphetamine use disorder: current status and future directions.Journal of neuroinflammation · 2025Review
- Porphyromonas gingivalis and Its Outer Membrane Vesicles Induce Neuroinflammation in Mice Through Distinct Mechanisms.Immunity, inflammation and disease · 2025Article
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- Illicit Drugs in Surface Waters: How to Get Fish off the Addictive Hook.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Article
- Effect of aerobic exercise on brain metabolite profiles in the mouse models of methamphetamine addiction: LC-MS-based metabolomics study.BMC psychiatry · 2023Article
- Substance abuse and neurodegenerative diseases: focus on ferroptosis.Archives of toxicology · 2023Review
- Effect of Aerobic Exercise on Intestinal Microbiota with Amino Acids and Short-Chain Fatty Acids in Methamphetamine-Induced Mice.Metabolites · 2023Article
- Identification ofFrontiers in pharmacology · 2023Article
- Increased Lipid Peroxidation and Lowered Antioxidant Defenses Predict Methamphetamine Induced Psychosis.Cells · 2022Article
- Effects of Aerobic Exercise on Markers of Brain Injury in Methamphetamine-Dependent Individuals: A Randomized Controlled Trial.Brain sciences · 2022Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThere is no effective therapeutic intervention developed targeting cerebrovascular toxicity of drugs of abuse, including methamphetamine (METH). We hypothesize that exercise protects against METH-induced disruption of the blood-brain barrier (BBB) by enhancing the antioxidant capacity of cerebral microvessels and modulating caveolae-associated signaling. Mice were subjected to voluntary wheel running for 5 weeks resembling the voluntary pattern of human exercise, followed by injection with METH (10 mg/kg). The frequency, duration, and intensity of each running session were monitored for each mouse via a direct data link to a computer and the running data are analyzed by Clock lab™ Analysis software. Controls included mice sedentary that did not have access to running wheels and/or injections with saline.
resultsMETH induced oxidative stress in brain microvessels, resulting in up regulation of caveolae-associated NAD(P)H oxidase subunits, and phosphorylation of mitochondrial protein 66Shc. Treatment with METH disrupted also the expression and colocalization of tight junction proteins. Importantly, exercise markedly attenuated these effects and protected against METH-induced disruption of the BBB integrity.
conclusionsThe obtained results indicate that exercise is an important modifiable behavioral factor that can protect against METH-induced cerebrovascular toxicity. These findings may provide new strategies in preventing the toxicity of drug of abuse.
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