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