I see all these benefits of nicotine post-stroke. Does this latest refute them all? Well, first off the nicotine is smoking delivered in the latest. So I bet the title of this is totally wrong. Nicotine is probably not the culprit, smoking is. Bad research.
Nicotine Holds Promise for Stronger Stroke Recovery
Nicotine Patch Appears To Help Mild Cognitive Loss
Can nicotine protect the aging brain?
I'm going to do the nicotine patches for my next stroke even though I have no clue on dosage. Don't listen to me with no medical training.
Abstract TP124: Nicotine Alters Brain Energy Metabolism and Exacerbates Ischemic Brain Damage
Abstract
Background:
Smoking-derived nicotine (N) and oral contraceptives (OC) are known to
synergistically magnify the risk and severity of cerebral ischemia in
females. The underlying pathological mechanism remains elusive. Our
studies have shown that N toxicity is exacerbated by OC via altered
mitochondrial function, which involved a defect in activity of
cytochrome c oxidase, the terminal enzyme of the electron transport
chain. However, the effects of impaired mitochondrial function on brain
metabolism remain to be investigated. To understand the impact in brain
metabolisms, in the current study we investigated the global metabolomic
profile of brains of adolescent and adult female rats exposed to N +/-
OC.
Methods: Six and twelve weeks old Sprague-Dawley female rats were randomly (n = 8/group) exposed to either saline, N (4.5 mg/kg) +/- OC for 16-21 days. At the end of the treatment, brain tissue was harvested for metabolomic analysis (performed by Metabolon Inc.) The metabolomic profile was complemented with western blot analysis and enzyme activity measurements.
Results: Pathway enrichment analysis showed significant changes in energy metabolism (glycolysis and TCA cycle) and neurotransmitters in both adolescent and adult rats exposed to N, OC and N+OC in relation to saline treatment. The changes were more pronounced in adolescent rats with a significant decrease in glucose, glucose 6-phosphate, fructose-6-phosphate along with a significant increase in pyruvate in N and N+OC exposed groups when compared to saline (p<0.05), suggesting alterations in the glycolytic pathway. Western blot analyses of glycolytic enzymes support the observed metabolic changes.
Conclusion: Nicotine and N+OC exposure increased brain glycolysis in an age-dependent manner. Since glucose metabolism is critical for brain physiology, altered glycolysis deteriorates neural function thus exacerbating ischemic brain damage. Moreover, significant decrease in the neuroactive peptide GABA was observed in young female rats treated with N+OC when compared to saline group. Discerning the exact effects of N +/- OC on overall brain metabolism and the molecular mechanisms affecting mitochondrial function at different ages will open a new window for future therapeutic intervention.
Methods: Six and twelve weeks old Sprague-Dawley female rats were randomly (n = 8/group) exposed to either saline, N (4.5 mg/kg) +/- OC for 16-21 days. At the end of the treatment, brain tissue was harvested for metabolomic analysis (performed by Metabolon Inc.) The metabolomic profile was complemented with western blot analysis and enzyme activity measurements.
Results: Pathway enrichment analysis showed significant changes in energy metabolism (glycolysis and TCA cycle) and neurotransmitters in both adolescent and adult rats exposed to N, OC and N+OC in relation to saline treatment. The changes were more pronounced in adolescent rats with a significant decrease in glucose, glucose 6-phosphate, fructose-6-phosphate along with a significant increase in pyruvate in N and N+OC exposed groups when compared to saline (p<0.05), suggesting alterations in the glycolytic pathway. Western blot analyses of glycolytic enzymes support the observed metabolic changes.
Conclusion: Nicotine and N+OC exposure increased brain glycolysis in an age-dependent manner. Since glucose metabolism is critical for brain physiology, altered glycolysis deteriorates neural function thus exacerbating ischemic brain damage. Moreover, significant decrease in the neuroactive peptide GABA was observed in young female rats treated with N+OC when compared to saline group. Discerning the exact effects of N +/- OC on overall brain metabolism and the molecular mechanisms affecting mitochondrial function at different ages will open a new window for future therapeutic intervention.
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