Nicotine and Brain Functioning
Nicotine administration can improve cognitive decline and impairment by inhibiting Sirtuin 6, a stress‑responsive protein deacetylase, thereby decreasing neuronal apoptosis and improving neuronal survival, a quality which is most important in Alzheimer's disease (AD), memory impairment in Parkinson's disease (PD, Read more below) and dyskinesia (Read More, And more). Nicotine improves cognitive impairment by enhancing protein kinase B (also referred to as Akt) activity and stimulating phosphoinositide 3‑kinase/Akt signaling, which regulates learning and memory processes. Nicotine may also activate thyroid receptor signaling pathways to improve memory impairment caused by hypothyroidism.
In healthy individuals, nicotine may improve memory function through its effect on chromatin modification via the inhibition of histone deacetylases, which causes transcriptional changes in memory‑related genes.
Furthermore, nicotine improves memory impairment caused by sleep deprivation by enhancing the phosphorylation of calmodulin‑dependent protein kinase II, an essential regulator of cell proliferation and synaptic plasticity. Finally, nicotine administration has been demonstrated to rescue long‑term potentiation in individuals with sleep deprivation, AD, stress and hypothyroidism, primarily by desensitizing α7 nicotinic acetylcholine receptors. To conclude, nicotine has several cognitive benefits in healthy individuals, as well as in those with cognitive decline associated with age or brain deseases.
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Nicotine Anti-Inflammatory Benefits
Inflammation is a complex process involving multiple genes and signaling pathways. In the recent decade, the finding that pro-inflammatory responses are controlled by neural circuits has given birth to the new concept of “inflammatory reflex. The cholinergic anti-inflammatory pathway is the efferent or motor arm of the “inflammatory reflex”, the neural circuit that responds to and regulates the inflammatory response. It is well known that nicotine, as an agonist of nicotinic Acetylcholine Receptors (nAChR) found in the central and peripheral nervous system, muscle, and many other tissues of many organisms, stimulates the nicotinic acetylcholine receptor signaling anti-inflammatory pathway to reduce inflammatory responses. (Read more)
Nicotine is a lipophilic agent and can penetrate the cells independently on these special nAChR receptors. Therefore, nicotine could directly affect mitochondrial respiration, cell autophagy, and cell signaling molecules in an environment with proper pH (nicotine pKa = 7.9).
Yet another study showed that given at the right dose, nicotine provides for a "protective effect of nicotine in a murine model of viral myocarditis induced by coxsackievirus".

B3Nicotine also played different regulatory roles in ulcerative colitis, arthritis, periodontitis, sepsis, endotoxemia, multiple sclerosis, nasal eosinophilic inflammation, allergy, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, skin inflammation, placental inflammation, pancreatitis, Behçet’s disease, muscle inflammation, viral myocarditis, uveitis, experimental autoimmune encephalomyelitis, systemic lupus erythematosus, and so on (Figure 1)