|THC||alzheimers in vitro||Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids||Jun 2016|
|Cannabinoids such as tetrahydrocannabinol stimulate the removal of intraneuronal Abeta-, block the inflammatory response, and are protective.|
|THC||alzheimers in vitro||A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology||Oct 2008|
|Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Abeta- aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.|
|Pinene||alzheimers,parkinsons in vitro||Inhibition of Acetylcholinesterase Activity by Bicyclic Monoterpenoids||Feb 2005|
|alpha-pinene and (+)-3-carene were potent inhibitors of AChE.|
|CBN||alzheimers in mice||Cannabinol delays symptom onset in SOD1 (G93A) transgenic mice without affecting survival||Sept 2004|
Ingestion Method: 5 mg/kg/day|
We found that this treatment significantly delays disease onset by more than two weeks while survival was not affected. Further research is necessary to determine whether non-psychotropic cannabinoids might be useful in ameliorating symptoms in ALS.
|Linalool||alzheimers in mice via experiment||Linalool reverses neuropathological and behavioral impairments in old triple transgenic Alzheimer's mice.||Mar 2016|
Ingestion Method: 25mg/kg|
Together, our findings suggest that linalool reverses the histopathological hallmarks of AD and restores cognitive and emotional functions via an anti-inflammatory effect. Thus, linalool may be an AD prevention candidate for preclinical studies.
|CBD||alzheimers in vitro||Cannabidiol Modulates the Expression of Alzheimer's Disease-Related Genes in Mesenchymal Stem Cells.||Dec 2016|
Action Pathway: TRPV1|
In conclusion, we have found that pre-treatment with CBD prevented the expression of proteins potentially involved in tau phosphorylation and Abeta- production in GMSCs. Therefore, we suggested that GMSCs preconditioned with CBD possess a molecular profile that might be more beneficial for the treatment of AD.
|Linalool||alzheimers in mice via experiment||Protective effects of linalool against amyloid beta-induced cognitive deficits and damages in mice.||Apr 2017|
|LI could attenuate cognitive deficits induced by Abeta-, and the neuroprotective effect of LI might be mediated by alleviation of apoptosis, oxidative stress depending on activation of Nrf2/HO-1 signaling. We could assume that LI has the potential to be a neuroprotective substance for AD therapy.|
|Linalool||alzheimers in mice via experiment||The Protective Effect of Lavender Essential Oil and Its Main Component Linalool against the Cognitive Deficits Induced by D-Galactose and Aluminum Trichloride in Mice.||2017|
Ingestion Method: 100 mg/kg|
Our results revealed that LO (100 mg/kg) or LI (100 mg/kg) significantly protected the cognitive impairments as assessed by the Morris water maze test and step-though test. The mechanisms study demonstrated that LO and LI significantly protected the decreased activity of superoxide dismutase (SOD), glutathione peroxidase (GPX), and protected the increased activity of acetylcholinesterase (AChE) and content of malondialdehyde (MDA).
|CBD||alzheimers,neuroprotective in vitro via experiment||Cannabidiol Reverses Deficits in Hippocampal LTP in a Model of Alzheimer's Disease.||Mar 2019|
Action Pathway: PPAR?|
However in the presence of the PPAR? antagonist GW9662 the neuroprotective effect of CBD was prevented. Our data suggests that this major component of Cannabis sativa, which lacks psychoactivity may have therapeutic potential for the treatment of AD.
|THC,CBN||alzheimers in model via model||Efficacy of Cannabinoids in a Pre-Clinical Drug-Screening Platform for Alzheimers Disease||May 2019|
|Positive Pairwise combinations of THC and CBN lead to a synergistic neuroprotective interaction. Together, these results significantly extend the published data by showing that non-psychoactive cannabinoids are potential lead drug candidates for AD and other neurodegenerative diseases.|
|cannabinoids||alzheimers in mice||CB2 Cannabinoid receptor agonist ameliorates novel object recognition but not spatial memory in transgenic APP/PS1 mice||May 2019|
Action Pathway: CB2|
Our results demonstrated that CB2R activation exerts a beneficial role in novel object recognition ability concomitant with region-specific regulation in microglia-mediated neuroinflammation and dendritic complexity in AD-model mice.