A new study conducted by researchers at the Roskamp Institute in Florida, and published in the journal Molecular and Cellular Neuroscience, has found that cannabis can slow the effects of Alzheimer’s Disease, and may in fact be able to halt it entirely.
According to Corbin Bachmeier, Ph.D – who’s the lead researcher of the study – Alzheimer’s Disease is “the result of impaired Aβ [Amyloid-β protein] clearance from the brain”. According to this study, cannabis can solve this problem, making it a potential treatment.
Here’s the study’s abstract:
Emerging evidence suggests beta-amyloid (Aβ) deposition in the Alzheimer’s disease (AD) brain is the result of impaired clearance, due in part to diminished Aβ transport across the blood–brain barrier (BBB). Recently, modulation of the cannabinoid system was shown to reduce Aβ brain levels and improve cognitive behavior in AD animal models. The purpose of the current studies was to investigate the role of the cannabinoid system in the clearance of Aβ across the BBB. Using in vitro and in vivo models of BBB clearance, Aβ transit across the BBB was examined in the presence of cannabinoid receptor agonists and inhibitors. In addition, expression levels of the Aβ transport protein, lipoprotein receptor-related protein1 (LRP1), were determined in the brain and plasma of mice following cannabinoid treatment. Cannabinoid receptor agonism or inhibition of endocannabinoid-degrading enzymes significantly enhanced Aβ clearance across the BBB (2-fold). Moreover, cannabinoid receptor inhibition negated the stimulatory influence of cannabinoid treatment on Aβ BBB clearance. Additionally, LRP1 levels in the brain and plasma were elevated following cannabinoid treatment (1.5-fold), providing rationale for the observed increase in Aβ transit from the brain to the periphery. The current studies demonstrate, for the first time, a role for the cannabinoid system in the transit of Aβ across the BBB. These findings provide insight into the mechanism by which cannabinoid treatment reduces Aβ burden in the AD brain and offer additional evidence on the utility of this pathway as a treatment for AD.