Cited by 123Alzheimer's disease research and treatmentsCannabis and Cannabinoid ResearchMedicinal Plants and Neuroprotection

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The potential therapeutic effects of THC on Alzheimer’s disease

Cao, Chuanhai, Li, Yaqiong, Liu, Hui, Bai, Ge, Mayl, Jonathan, Lin, Xiaoyang, Sutherland, Kyle, Nabar, Neel, Cai, Jianfeng·2014·Journal of Alzheimer s Disease

DOI 10.3233/jad-140093

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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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Authors: Cao, C., Li, Y., Liu, H., Bai, G., Mayl, J., Lin, X., Sutherland, K., Nabar, N., & Cai, J.
Affiliations: University of South Florida (US)
Thomas Jefferson University (US)
ORCID: Cao, Chuanhai
Li, Yaqiong
Liu, Hui
Bai, Ge
Mayl, Jonathan
Nabar, Neel
Cai, Jianfeng
Venue: Journal of Alzheimer s Disease
Publisher: SAGE Publications
Published: 2014-09-16
Volume: 42
Issue: 3
Pages: 973-984
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-140093
OpenAlex: W2132194615
Cited by: 121
References: 42
Citations by year: 2026: 6 · 2025: 10 · 2024: 6 · 2023: 14 · 2022: 27 · 2021: 11 · 2020: 11 · 2019: 6 · 2018: 8 · 2017: 7 · 2016: 7 · 2015: 6 · 2014: 2
FWCI: 5.10
Type: journal article
Language: en
Open access: closed
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords: delta-9-tetrahydrocannabinol, Alzheimer's disease
MeSH terms: Glycogen Synthase Kinase 3 beta, Animals, Dose-Response Relationship, Drug, Enzyme-Linked Immunosorbent Assay, Humans, Mitochondria, Mutation, Neuroblastoma, Phosphorylation, Dronabinol, Transfection, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Cell Respiration, Glycogen Synthase Kinase 3, Cell Line, Tumor, Mice, Cannabinoid Receptor Agonists

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