Nicotine and inflammatory neurological disorders

[SilentEchoes]

There is increasing evidence that smokers have a lower incidence of some inflammatory and neurodegenerative diseases. Nicotine is immunosuppressive, which inhibits both the innate and adaptive immune responses.

Nicotine is not yet considered to be a carcinogen and may, in fact, have therapeutic potential as a neuroprotective and anti-inflammatory agent. A multitude of studies suggest that nicotine, a psychoactive component of tobacco products, acts in a similar fashion as the naturally occurring neurotransmitter, acetylcholine, on nicotinic acetylcholine receptors (nAChRs) found in many organ systems and has profound immunological effects.

Epidemiological studies have shown an association of smoking with a lower occurrence of PD. Nicotine activates the striatal or mesolimbic dopaminergic system and protects against glutamate-induced neurotoxicity in striatal, cortical and mesencephalic neurons, as well as nigrostriatal degeneration in MPTP-treated animals. Nicotine could suppress the formation of toxin by directly influencing enzyme activities, such as monoamine oxidases (MAO). Nicotine might also modulate the members of the cytochrome P450 (CYP) family [detox pathway]. Furthermore, nicotine could act by modulating mitochondrial complex Ι activity to preserve mitochondrial function and consequently reduce neuronal damage.

Numerous signaling pathways are altered in response to nACh receptor activation, including presynaptic pathways involved in control of neurotransmitter release (dopamine, ACh, GABA, and glutamate) and postsynaptic pathways involved in apoptosis (phospholipase C, arachidonic acid, reactive oxygen species, neuronal nitric oxide synthase, and cGMP) and necrosis (phospholipase C, protein kinase C, MAPK, ERK, and Bcl2), immune modulation (IL-1, IL-6, and TNFα) and neurotrophic factor production (brain derived neurotrophic factor, fibroblast growth factor 2). Activation of these pathways might subsequently lead to neuroprotection through inhibition of toxin-induced apoptosis, and increased expression of neurotrophic factors, which are crucial for neuronal maintenance, survival and regeneration.

You can read the entire study here: ncbi.nlm.nih.gov/labs/pmc/a...

SE

[JayPwP]

Interesting...

[Despe]

Have you tried it? If not, will you, SE?

[SilentEchoes in reply to Despe]

A few years ago I tried the patch just briefly. I'm a non-smoker, it seemed weird to me. I understand the concepts of neuroinflammation and excitotoxicity better now. Going to restart. Never smoked pot either, I'm legal now 🙂 my kids don't know what do about me, lol.

[Despe]

👍😀

[kaypeeoh]

I've never smoked and but trying a STOP Smoking patch now. I cut it into 1/4 pieces and stick on my arm. So far the only problem is I don't like the smell. It's not onerous, just annoying. I'm trying it because of possible neurocognitive disorder. I don't feel that I have this but it can't hurt to try.

[Bundoran]

Smoke cigars instead of ciggies. Cigarettes are inhaled into the lungs for quick absorption of nicotine. Cigar smoke is not inhaled but is rolled around the mouth with the nicotine absorbed through the pallete. It's a slower process and it takes longer. Smoking also helps with constipation. The downside, cigars are expensive.

[SilentEchoes in reply to Bundoran]

Um, no. I'll get it in anyway I can but inhaling - chemical sensitivity