06 Feb UT Health San Antonio Study Finds Lows Dose THC Plus Celecoxib May Prevent or Delay Onset of Alzheimer’s Disease

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MedicalResearch.com Interview with:

Prof. Chu Chen

Chu Chen, PhD
Professor and Joe R. and Teresa Lozano Long Chair in Neural Physiology
Department of Cellular and Integrative Physiology
Center for Biomedical Neuroscience
Joe R. and Teresa Lozano Long School of Medicine
University of Texas at San Antonio Health Science Center
San Antonio, TX 78229

MedicalResearch.com: What is the background for this study?

Response: Alzheimer’s disease (AD) is the most common cause of dementia in the elderly, yet no effective therapies currently exist to prevent, treat, or halt its progression. Cannabis has been used for thousands of years for both recreational and medicinal purposes; however, its therapeutic application has been limited by undesirable neurocognitive side effects, particularly impairments in learning and memory. Δ9-Tetrahydrocannabinol (Δ9-THC), the primary psychoactive component of cannabis, has been shown to reduce amyloid-β (Aβ) pathology in animal models of AD, but at high doses (>5.0 mg/kg) it also disrupts synaptic function and impairs cognition.

Research from our laboratory and others has demonstrated that Δ9-THC-induced deficits in long-term synaptic plasticity, learning, and memory are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid into pro-inflammatory prostaglandins. Notably, pharmacological inhibition or genetic deletion of COX-2 attenuates Δ9-THC-induced synaptic and cognitive impairments. Based on these findings, we proposed a combination (“cocktail”) therapy consisting of low-dose Δ9-THC and the anti-inflammatory drug celecoxib, a selective COX-2 inhibitor, as a potential therapeutic strategy for AD. This approach is designed to preserve the beneficial effects of Δ9-THC while minimizing its adverse neurocognitive effects and COX-2-mediated inflammatory responses.

MedicalResearch.com: What are the main findings?

• Δ9-THC (3.0 mg/kg), administered alone or in combination with celecoxib (1.0 mg/kg) before symptom onset, significantly reduced amyloid-β (Aβ) and tau pathologies, enhanced synaptic marker expression, and prevented the onset of cognitive decline.
• The combination treatment produced greater improvements in spatial learning and effectively mitigated Δ9-THC-induced neuroinflammatory responses.
• Δ9-THC reversed or attenuated dysregulated expression of synaptic and immune/inflammation-related genes and restored the downregulated expression of genes associated with Alzheimer’s disease observed in both AD patients and AD animal models, with greater efficacy when combined with celecoxib in AD model animals.
• Collectively, these findings suggest that low-dose Δ9-THC combined with celecoxib can prevent or delay the onset of Alzheimer’s disease.

MedicalResearch.com: What could be the mechanism for this effect? 

Response:  Δ9-THC, administered alone or in combination with celecoxib, reduces the expression of enzymes involved in amyloid-β (Aβ) synthesis while enhancing the expression of the enzyme responsible for Aβ clearance; decreases phosphorylated tau and inflammatory mediators associated with AD pathology and Δ9-THC-induced COX-2 activation; preserves synaptic integrity; and attenuates or reverses dysregulated gene expression related to synaptic function, inflammation, and Alzheimer’s disease.

MedicalResearch.com: Are there risks of side effects from either/both of these meds?

Response:  We cannot rule out the possibility of side effects from one or both medications used in this study. In particular, the long-term safety of using this combination, how well it works overtime, and whether there could be cumulative effects with prolonged use still need to be carefully studied. That said, the doses of Δ9-THC and celecoxib used in our research were relatively low and are generally considered safe based on existing clinical experience. For this reason, we believe this combination may have a favorable safety profile.
However, any use of these medications should occur only under the guidance and supervision of a qualified healthcare professional. 

MedicalResearch.com: What should readers take away from your report?

Response: In this study, we administered Δ9-THC alone or in combination with celecoxib to animal models of Alzheimer’s disease (AD) prior to the development of synaptic and cognitive impairments and conducted assessments at time points when these symptoms had emerged. Based on the results of the present study, this combination therapy may prevent or delay the onset of Alzheimer’s disease in AD animal models.

A key advantage of this approach is that both Δ9-THC (in the form of dronabinol or nabilone) and celecoxib are FDA-approved medications already in clinical use; therefore, this combination therapy could be rapidly advanced to clinical trials to evaluate its efficacy in preventing or delaying AD onset in humans, should clinical groups be interested in initiating such trials.

Importantly, any use of these medications should occur only under the guidance and supervision of a qualified healthcare professional.

MedicalResearch.com: What recommendations do you have for future research as a results of this study?

Response: As described above, the treatment in the current study was administered before the appearance of Alzheimer’s disease-related neuropathology and cognitive decline, suggesting that this combination therapy has the potential to prevent or delay the onset of Alzheimer’s disease. However, it remains unclear whether this combination therapy can delay, halt, or reverse disease progression when administered after Alzheimer’s symptoms have emerged. Therefore, as a next step, we propose to determine whether combined administration of Δ9-THC and celecoxib at symptomatic stages can reverse or slow disease progression in AD animal models, contingent upon the successful acquisition of funding support.

Disclosures: The patents covering the combination therapy of Δ9-THC and celecoxib was granted by the United States Patent and Trademark Office in 2017.

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Last Updated on February 6, 2026 by Marie Benz MD FAAD