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Nicotine's Therapeutic Effects

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Nicotine's Therapeutic Effects
Nicotine has been used since the 1800s for cultural activities and therapeutic effects. The American Indians used tobacco with nicotine as a powerful insecticide for seed protection and as a human vermifuge. The Shamans used high doses of nicotine to induce catatonic state intoxication which represented symbolic death. Due to the short half-life and quick elimination of nicotine, these people returned to full consciousness after a few hours. Nicotine is currently being tested for its medical therapeutic effects. Studies conducted thus far have shown nicotine to have therapeutic effects in Gilles de la Tourette's syndrome, depression, and schizophrenia (12).
Epidemiological studies have shown that depressed patients have a higher smoking prevalence
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This neuroprotective effect has shown to be beneficial to patients diagnosed with PD (22). Nicotine’s positive effect on motor coordination and behavior is due to its ability to increase dopamine availability while reducing the production of reactive oxygen species. Nicotinic acetylcholine receptors (nAChRs) activation is considered the mechanism of action of nicotine against PD (4). Neuronal nAChR's are quantitatively reduced in patients of neurodegenerative disease so nicotine allows a stronger signal to these receptors. These receptors regulate synaptic transmission and plasticity in several regions of the brain including the midbrain dopamine centers. When these ligand-gated receptors are activated, they cause depolarization and the increase of both intraneuronal calcium levels and neurotransmitter release probability. Activation of nAChRs allows for the prevention of neurodegeneration by mechanisms involving the activation of pro-survival signaling factors (14).
Nicotine can also stimulate cholinergic anti-inflammatory pathways (11). The vagus nerve can cause peripheral release of acetylcholine that in turn activates the cholinergic receptors in the brain. The release of acetylcholine inhibits activity of pro-inflammatory nuclear factor kappa B (NFkB) in macrophages. The expression of cytokines, such as tumor necrosis factor (TNF), are also consequently inhibited

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