Alzheimer's - Dementia, Author Interviews, Cannabis / 06.02.2026
UT Health San Antonio Study Finds Lows Dose THC Plus Celecoxib May Prevent or Delay Onset of Alzheimer’s Disease
Editor's note: Do Not Use these products alone or in combination without the specific guidance of your health are provider, due to risks of untoward side effects.
THC/CBD and other cannabis products should not be used if you are pregnant, planning to become pregnant or nursing. Children should not be exposed to cannabis in any form.
MedicalResearch.com Interview with:
[caption id="attachment_72277" align="alignleft" width="200"]
Prof. Chu Chen[/caption]
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.
Prof. Chu Chen[/caption]
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.
