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:
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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.
Dr. Guasch-Ferré[/caption]
Marta Guasch-Ferré, PhD
Associate Professor and Deputy Head of Section, Section of Epidemiology
University of Copenhagen
Group Leader, Novo Nordisk Foundation Center for Basic Metabolic Research
Adjunct Associate Professor, Department of Nutrition
Harvard TH Chan School of Public Health
MedicalResearch.com: What is the background for this study?
Response: Olive oil is rich in monounsaturated fats and contains compounds with antioxidant activity that may play a protective role for the brain. Olive oil as part of a Mediterranean diet appears to have a beneficial effect against cognitive decline. Higher olive oil intake was previously associated with a lower risk of cardiovascular disease and mortality. But its association with dementia mortality was unknown.
Dr. Li Gan[/caption]
Dr. Li Gan PhD
Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases
Brain and Mind Research Institute
Weill Cornell Medical College
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Dr. Dolatshahi[/caption]
Mahsa Dolatshahi, M.D., M.P.H.
Post-doctoral research fellow
Mallinckrodt Institute of Radiology (MIR)
Washington University School of Medicine
St. Louis
MedicalResearch.com: What is the background for this study?
Response: Obesity at midlife is recognized as a risk factor for developing Alzheimer disease decades afterwards. However, body mass index on its own does not adequately represent the risks associated with obesity.
In this study, we went beyond BMI and considered anatomical distribution of body fat, including the metabolically active visceral fat in the belly, and showed its association with Alzheimer pathology in the form of amyloid proteins. In addition, visceral fat along with obesity and insulin resistance were associated with thinning of brain cortex, as early as midlife.
Dr. Belloy[/caption]
Michael E. Belloy, PhD
Department of Neurology and Neurological Sciences
Stanford University, Stanford, California
MedicalResearch.com: What is the background for this study?
Response: Apolipoprotein E (APOE)*2 and APOE*4 are, respectively, the strongest protective and risk-increasing, genetic variants for late-onset Alzheimer disease. As such, one’s APOE genotype is highly relevant towards clinical trial design and Alzheimer’s disease research. However, most insights so far are focused on the associations of these APOE genotypes with Alzheimer’s disease risk in non-Hispanic white individuals.
One important aspect of our work is that we really increased sample sizes for non-Hispanic Black, Hispanic, and East Asian individuals, so that we now have better understanding of the associations of APOE genotypes with Alzheimer’s disease risk in these groups. In complement, we also did the largest investigation to date on the role of ancestry on the associations of APOE genotypes with Alzheimer’s disease risk. The scale of our study was thus a critical factor in generating novel insights.
Dr. Manson[/caption]
JoAnn E. Manson, MD, DrPH, MACP
Julia Cave Arbanas[/caption]
Julia Cave Arbanas
Project Manager and
Dr. Martens[/caption]
Christopher R. Martens PhD
Assistant Professor
Director, Delaware Center for Cognitive Aging Research
Department of Kinesiology & Applied Physiology
University of Delaware
Newark, DE
MedicalResearch.com: What is the background for this study?
Response: One of the main issues with Alzheimer's disease is an impaired ability to make energy in the brain. NAD+ is critically involved in the creation of energy within cells and there is strong evidence that nicotinamide riboside (NR), a precursor to NAD+, can restore brain function in mice that exhibit similar characteristics as people with Alzheimer's disease.
We had previously studied the effects of NR in healthy older adults and wanted to see whether it is even capable of getting into brain tissue. We used remaining blood samples from our original study and measured the amount of NAD+ within tiny "vesicles" in the blood that we are quite confident originated from the brain and other neural tissue
