User:Tkadm30/Notebook/THC: Difference between revisions
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===Anticholinergic properties of THC=== | ===Anticholinergic properties of THC=== | ||
* THC inhibit anticholinesterase (AChE) induced beta-amyloid aggregation in Alzheimer's disease: | * THC inhibit anticholinesterase (AChE) induced beta-amyloid aggregation in Alzheimer's disease: <cite>Eubanks-2006</cite> | ||
* THC as antiglutamatergic therapy for AChE induced neurotoxicity: [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891218/ PMID] [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366364/ PMID] [https://www.ncbi.nlm.nih.gov/pubmed/18680758 PMID] | * THC as antiglutamatergic therapy for AChE induced neurotoxicity: [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2891218/ PMID] [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366364/ PMID] [https://www.ncbi.nlm.nih.gov/pubmed/18680758 PMID] | ||
* Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE | * Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE | ||
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===References=== | ===References=== | ||
<biblio> | <biblio> | ||
#Eubanks-2006 pmid=17140265 | |||
//A molecular link between the active component of marijuana and Alzheimer's disease pathology. | |||
#Website1 https://en.wikipedia.org/wiki/Cannabinoid | #Website1 https://en.wikipedia.org/wiki/Cannabinoid | ||
#Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ | #Website2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2866040/ | ||
Revision as of 05:24, 16 November 2015
Synopsis
- Tetrahydrocannabinol (THC) is the main psychoactive constituent of Cannabis sativa L (Marijuana) plant.
- Other Marijuana compounds includes Cannabichromene (CBC), Cannabidiol (CBD), Cannabinol (CBN), and Cannabigerol (CBG).
- Cannabis-derived cannabinoids are known as phytocannabinoids.
- THC stimulate anandamide biosynthesis by binding to the CB1 receptor, thus producing a antidepressant and neuroprotective effect. [1]
Anticholinergic properties of THC
- THC inhibit anticholinesterase (AChE) induced beta-amyloid aggregation in Alzheimer's disease: [2]
- THC as antiglutamatergic therapy for AChE induced neurotoxicity: PMID PMID PMID
- Unlike THC, caffeine is a noncompetitive reversible inhibitor of AChE
Proneurogenic effect of THC on neurogenesis
- Regulation of stress-induced neuroinflammation in the hippocampus.
- Hippocampal neurogenesis is enhanced. PMID PMID
- CB1 activation promote neuronal cell proliferation, differentiation, maturation, and neurite growth. PMID
Experimental
- Synaptogenic effect of Δ9-THC/DHEA ligands promote hippocampal development.
- Δ9-THC/DHEA ligands (synaptamide) affect neural stem/progenitor cells (NS/PC) proliferation in the hippocampus.
References
- Eubanks LM, Rogers CJ, Beuscher AE 4th, Koob GF, Olson AJ, Dickerson TJ, and Janda KD. A molecular link between the active component of marijuana and Alzheimer's disease pathology. Mol Pharm. 2006 Nov-Dec;3(6):773-7. DOI:10.1021/mp060066m |
A molecular link between the active component of marijuana and Alzheimer's disease pathology.
