[ExI] Alzheimer's and pot

[Keith Henson]

http://www.ncbi.nlm.nih.gov/pubmed/25024327#

I was just going to send this to Spike, but it's one of the things
many of us tend to be concerned about.

Keith

The potential therapeutic effects of THC on Alzheimer's disease.

Cao C1, Li Y2, Liu H1, Bai G2, Mayl J3, Lin X1, Sutherland K4, Nabar N5, Cai J2.

Author information

Abstract

The purpose of this study was to investigate the potential therapeutic
qualities of Δ9-tetrahydrocannabinol (THC) with respect to slowing or
halting the hallmark characteristics of Alzheimer's disease.
N2a-variant amyloid-β protein precursor (AβPP) cells were incubated
with THC and assayed for amyloid-β (Aβ) levels at the 6-, 24-, and
48-hour time marks. THC was also tested for synergy with caffeine, in
respect to the reduction of the Aβ level in N2a/AβPPswe cells. THC was
also tested to determine if multiple treatments were beneficial. The
MTT assay was performed to test the toxicity of THC. Thioflavin T
assays and western blots were performed to test the direct anti-Aβ
aggregation significance of THC. Lastly, THC was tested to determine
its effects on glycogen synthase kinase-3β (GSK-3β) and related
signaling pathways. From the results, we have discovered THC to be
effective at lowering Aβ levels in N2a/AβPPswe cells at extremely low
concentrations in a dose-dependent manner. However, no additive effect
was found by combining caffeine and THC together. We did discover that
THC directly interacts with Aβ peptide, thereby inhibiting
aggregation. Furthermore, THC was effective at lowering both total
GSK-3β levels and phosphorylated GSK-3β in a dose-dependent manner at
low concentrations. At the treatment concentrations, no toxicity was
observed and the CB1 receptor was not significantly upregulated.
Additionally, low doses of THC can enhance mitochondria function and
does not inhibit melatonin's enhancement of mitochondria function.
These sets of data strongly suggest that THC could be a potential
therapeutic treatment option for Alzheimer's disease through multiple
functions and pathways.

KEYWORDS:

Alzheimer's disease; CB1 receptor; CB2 receptor; amyloid-β peptide;
cannabinoid; delta(9)-tetrahydrocannabinol; neurodegeneration