The Therapeutic Potential of CBD and THC in Alzheimer’s Disease: A Comprehensive Review
Haya Nasr, Andrew Roden, and Ciantel Velo
Undergraduate Students, University of Guelph
1. Introduction
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and significant behavioural changes. Current treatments offer only modest symptom relief and do little to alter pathological processes, prompting increasing interest in multi-target therapeutic strategies (Ahmed et al., 2015). Cannabinoids are bioactive compounds derived from Cannabis sativa, are synthesized endogenously or produced synthetically. They have emerged as promising candidates because they interact with the endocannabinoid system (ECS), a regulatory network involved in mood, inflammation, and neuronal signalling (Abodeely, 2023; Li et al., 2023).
THC and CBD are the two best-studied phytocannabinoids, they differ in psychoactivity, receptor affinity, metabolism, and safety profiles. THC primarily activates CB1 receptors, while CBD modulates CB2 and non-cannabinoid targets relevant to inflammation, oxidative stress, and synaptic stability (Ahmed et al., 2015; Li et al., 2023; Stella, 2023). These mechanisms overlap significantly with processes disrupted in AD, including amyloid-β accumulation, tau hyperphosphorylation, microglial activation, and glutamatergic dysfunction (Li et al., 2023; Ramírez et al., 2005; Solas et al., 2013).
Understanding the botanical and biochemical origins of cannabinoids is essential for evaluating their potential in AD therapy. Cannabinoid distribution varies across Cannabis species and plant structures, with the highest concentrations found in trichomes of female flowers (Sensi Seeds, 2022; Talei et al., 2025). Cultivation and propagation methods, including cloning and tissue culture, play a critical role in producing consistent cannabinoid profiles necessary for medical applications (Talei et al., 2025).
Preclinical studies demonstrate that cannabinoids can modulate inflammation, improve synaptic function, and reduce AD-related pathology (Coles et al., 2022; Li et al., 2023; Sánchez-Fernández et al., 2024). Early clinical evidence suggests potential benefits for agitation and cognitive stabilization (Cury et al., 2025; Herrmann et al., 2019; Johns Hopkins Medicine, 2024). However, these possibilities raise ethical questions concerning informed consent, psychoactivity, patient vulnerability, and caregiver decision-making.
This paper integrates botanical, pharmacological, ethical, and clinical perspectives to evaluate whether cannabinoids represent a scientifically plausible and ethically responsible avenue for Alzheimer’s disease treatment.
2. Cannabinoids: Overview
2.1 What Cannabinoids Are
Cannabinoids are compounds that interact with the ECS, a network in the body that regulates functions such as mood, appetite, pain, and sleep (Abodeely, 2023; Ahmed et al., 2015). They can be classified into three types: phytocannabinoids (plant-derived), endocannabinoids (produced naturally by the body), and synthetic cannabinoids (created in the laboratory to mimic or modify natural compounds).
Phytocannabinoids originate mainly from cannabis plants, endocannabinoids are synthesized on demand within the nervous and immune systems, and synthetic cannabinoids are primarily used in research and pharmaceutical contexts (Abodeely, 2023; Li et al., 2023). Defining these categories provides a foundation for understanding how different cannabinoids influence brain function and their potential therapeutic applications, explored in later sections.
2.2 THC vs CBD
The two most studied cannabinoids, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), differ in their psychoactive properties and receptor interactions. THC is psychoactive and primarily activates CB1 receptors, whereas CBD is non-psychoactive and interacts with CB2 and other receptors (Ahmed et al., 2015; Li et al., 2023). Both compounds are lipophilic metabolites of resorcinol and contribute to ECS regulation (Ahmed et al., 2015). THC can be inhaled for rapid brain penetration or ingested orally for slower, prolonged exposure, producing active metabolites such as 11-hydroxy-THC (Stella, 2023). These pharmacokinetic differences are relevant for evaluating dosing, safety, and potential therapeutic roles discussed in Section 4. Although THC and CBD have distinct biological properties, their therapeutic potential relates to complementary effects on inflammation, neurotransmission, and cell-signalling pathways.
2.3 How Cannabinoids Work in the Brain
Cannabinoids influence brain function primarily through CB1 and CB2 receptors, which regulate neurotransmission, synaptic plasticity, and neuroimmune activity (Ahmed et al., 2015; Stella, 2023). CB1 receptors (abundant in the cortex, hippocampus, basal ganglia, and cerebellum) reduce glutamate, GABA, acetylcholine, and dopamine release, affecting mood, cognition, memory, sleep, and motor control. CB2 receptors are low in healthy brain tissue but upregulate in microglia during inflammation, regulating immune signalling. Cannabinoids also interact with glycine receptors, GPR55, TRPV1, and serotonergic receptors, with effects dependent on dose and context.
3. Cannabis Plant: Botany & Cultivation
3.1 Plant Biology: Species, Structure, & Cannabinoid Distribution
Cannabis is generally classified into three species: sativa, indica, and ruderalis (Shango, 2023; Talei et al., 2025) (Figure 1). Sativa plants are tall with thin leaves, thrive in hot, dry climates, and have higher THC levels, producing stimulating effects. Indica plants are shorter, bushier, and often contain more CBD than THC, associated with relaxing effects. Ruderalis plants are small and low in THC and CBD, mainly used in hybrid breeding. Cannabis is an annual, dioecious plant with male and female flowers on separate plants. Occasionally, plants may be monoecious or hermaphroditic (Talei et al., 2025).
Figure 1. Subspecies of Cannabis sativa (McPartland, 2018).
The main structure of the cannabis plant includes roots, stems, leaves, flowers, trichomes, and seeds. Roots consist of a strong taproot branching 30-60 cm deep, while stems are erect, furrowed, and branched. Leaves are palmate with serrated edges. Their size and shape vary by species, with sativa leaves thinner and indica leaves broader and darker.
Cannabinoids are concentrated in specific tissues, particularly in female reproductive structures. The flowers are the primary site of cannabinoid production, with glandular trichomes on bracts and floral leaves serving as the biochemical factories (Sensi Seeds, 2022). These trichomes synthesize cannabinoid acids (THCA, CBDA), which convert into active cannabinoids (THC, CBD) through heat or aging. They also produce terpenes and flavonoids that contribute to aroma and therapeutic effects (Sensi Seeds, 2022; Talei et al., 2025). Sugar leaves near the flowers contain moderate cannabinoid levels, while stems and seeds contain negligible amounts.
Overall, cannabinoid distribution is highest in glandular trichomes of female flowers, which explains why medical and recreational use focus on flowering tops.
3.2 Cultivation & Propagation
Cannabis is propagated either sexually through seeds or asexually through cloning (Talei et al., 2025). Seeds maintain genetic diversity but produce variable cannabinoid content, while clones preserve desirable traits and ensure consistent cannabinoid profiles. Cloning uses cuttings from a selected female plant to produce genetically identical offspring, making it the preferred approach in medical and recreational cannabis production (Talei et al., 2025). Clones are typically grown indoors or in greenhouses where light cycles, temperature, humidity, and nutrient availability can be controlled to optimize growth. Advanced propagation techniques enable the mass production of disease-free, genetically uniform plants. Micropropagation supports the conservation of high-quality genotypes and scalability for pharmaceutical applications (Talei et al., 2025). Overall, propagation choices balance cost, consistency, and quality.
4. Medicinal Significance of Cannabinoids
4.1 Mechanisms Relevant to Alzheimer’s Disease
Cannabinoids influence several pathways involved in AD, including amyloid-β (Aβ) and tau pathology, neuroinflammation, oxidative stress, excitotoxicity, mitochondrial function, and cholinergic signalling (Ahmed et al., 2015; Li et al., 2023; Stella, 2023). Many of these pathways involve the ECS, which becomes dysregulated during AD progression.
CB1 Receptors
CB1 receptors regulate synaptic activity in brain regions heavily affected by Alzheimer’s. In AD, CB1 expression decreases in some areas, but higher CB1 levels in the frontal cortex correlate with better cognitive performance (Lee et al., 2010). Activation of CB1 can reduce Aβ accumulation, protect synapses, and modulate glutamate-related excitotoxicity.
CB2 Receptors
CB2 receptors are normally low in the CNS but increase dramatically in microglia surrounding Aβ plaques in AD (Li et al., 2023; Ramírez et al., 2005; Solas et al., 2013). This upregulation reflects AD-associated inflammation, and CB2 activation can shift microglia from a pro-inflammatory phenotype toward a more protective state (Solas et al., 2013). CB2 signalling promotes Aβ clearance, reduces oxidative stress, suppresses cytokine release, and decreases tau phosphorylation, making CB2 a promising therapeutic target.
THC
THC influences several AD-related pathways. It reduces Aβ aggregation, inhibits acetylcholinesterase (AChE), and decreases GSK-3β activity, a key driver of tau hyperphosphorylation (Li et al., 2023; Stella, 2023). Supporting these findings, a study (Eubanks et al., 2006) showed that THC binds to the peripheral anionic site of AChE, completely blocking its ability to promote Aβ fibril formation. It was more effective than both the PAS ligand propidium and FDA-approved AD drugs, suggesting it can directly modulate a key molecular driver of AD pathology while also addressing cholinergic deficits.
CBD
CBD contributes to neuroprotection through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms (Iuvone et al., 2004; Li et al., 2023; Stella, 2023). It stabilizes intracellular calcium, protects neurons from oxidative stress, reduces tau hyperphosphorylation, and limits microglia-mediated neurotoxicity. Additional in vitro evidence shows that CBD also downregulates β- and γ-secretase genes and reduces APP expression through PPARγ-mediated ubiquitination, further decreasing Aβ production (Coles et al., 2022) (Figure 2).
Figure 2. CBD and THC effects on amyloid, tau, and neuroprotection (Coles et al., 2022).
THC + CBD Combination
Low-dose THC combined with CBD improves outcomes more than either alone, reducing extracellular glutamate, normalizing hippocampal excitability, and enhancing cognition in AD models. THC can impair excitability at high doses, while CBD alone has limited cognitive effects, highlighting their complementary actions (Ahmed et al., 2015; Sánchez-Fernández et al., 2024).
Endocannabinoids
Endogenous cannabinoids such as 2-AG and anandamide also contribute to neuroprotection in AD models. They reduce apoptosis, limit neuroinflammation, prevent Aβ-induced neuronal damage, and support neurogenesis and memory function (Li et al., 2023; Ahmed et al., 2015).
Other Molecular Targets
Cannabinoids also affect other receptors and channels involved in AD, including glycine, TRPV1, GPR55, GABA_A, and 5-HT1A (Iuvone et al., 2004; Stella, 2023). These interactions can support synaptic stability, reduce excitotoxicity, and contribute to anxiolytic or anti-inflammatory effects. Minor cannabinoids (CBN, CBG, CBC, CBDV, THCA, CBDA) provide additional antioxidant and mitochondrial-protective actions against Aβ toxicity (Coles et al., 2022).
Summary
Overall, CB1 and CB2 receptors, along with THC and CBD, especially together, work in complementary ways to protect neurons and support brain function. These findings support cannabinoids as multi-target therapeutic candidates for AD.
4.2 Multi-Cannabinoid Treatments
Multi-cannabinoid approaches, particularly THC- CBD combinations, may improve therapeutic effects through synergistic interactions, often called the “entourage effect”. CBD can reduce negative psychological and cognitive effects of THC while also providing its own neuroprotective benefits. The overall effect depends on the dose, the ratio of cannabinoids, and how they are administered. Evidence from cell models, animal studies, and early clinical trials suggests that low-THC or balanced formulations may be better tolerated and more effective than single-compound treatments, although more research is required (Coles et al., 2022).
4.3 Animal Studies
Animal models, particularly APP/PS1 transgenic mice, are widely used to study how cannabinoids influence AD-related pathology. These mice develop amyloid deposition, synaptic dysfunction, and progressive cognitive impairment (Lok et al., 2013), making them suitable for testing cannabinoid effects across disease stages.
Early studies showed that long-term treatment with a combined THC-CBD formulation can normalize neuronal hyperexcitability, a process implicated in early AD progression (Sánchez-Fernández et al., 2024). In APP/PS1 mice, the combination reduced excessive extracellular glutamate in the hippocampus, even when glutamate release was experimentally amplified. This effect was not observed with either compound alone. This finding suggests synergistic stabilization of excitatory signalling and potential protection against excitotoxic damage.
A more recent study evaluated whether this combined formulation remains beneficial during later stages of Alzheimer’s pathology. In 12-month-old APP/PS1 mice, an age with clear cognitive impairment, five weeks of THC-CBD treatment improved performance in the object-recognition memory test without reducing amyloid burden or neuroinflammation (Aso et al., 2016). These findings suggest that cannabinoids may support cognition at advanced disease stages by modulating neurotransmission rather than directly altering core AD pathology. Synaptic protein analysis indicated changes in excitatory/inhibitory balance, supporting this mechanism.
CBD alone has also shown preventive effects. In a long-term study, chronic CBD administration from 2.5 to 10.5 months of age prevented the development of social-recognition memory deficits in APP/PS1 mice (Cheng et al., 2014). These improvements occurred independently of amyloid reduction and were linked to anti-inflammatory effects and changes in lipid-metabolism pathways. This suggests that CBD may act primarily on secondary processes that contribute to early cognitive decline.
Additional preclinical work supports these patterns: cannabinoids can reduce neuroinflammation, enhance neurogenesis, decrease oxidative stress, and improve learning in various AD models, although outcomes depend on compound, dose, and disease stage (Coles et al., 2022). CBD consistently shows anti-inflammatory and neuroprotective properties, while THC’s effects are dose-dependent, meaning that it’s beneficial at low levels but potentially impairing higher concentrations. Evidence for minor cannabinoids remains limited but points toward similar protective mechanisms.
4.4 Human & Clinical Studies
Clinical evidence for cannabinoid-based treatments in Alzheimer’s disease remains limited, but the quality of research has gradually improved. Human studies often investigate either plant-derived cannabinoids, such as THC and CBD, or synthetic analogs that mimic THC’s effects, including nabilone and dronabinol. These synthetic compounds are commonly used in clinical settings to manage behavioural and neuropsychiatric symptoms while allowing controlled dosing.
Early randomized trials (Bosnjak et al., 2021) found little evidence for cognitive benefit and only small, uncertain reductions in agitation. Sedation, particularly with nabilone, was the most consistently reported side effect. These studies were generally short, underpowered, and methodologically weak, highlighting the need for more rigorous research.
A more robust double-blind crossover RCT evaluated nabilone in 38 patients with moderate to severe AD (Herrmann et al., 2019). Nabilone significantly reduced agitation compared to placebo and improved overall neuropsychiatric symptoms and caregiver distress. Sedation remained the main side effect but was generally manageable with dose adjustments. This study provided early evidence that cannabinoids may have clinically relevant effects on agitation. Emerging trials have also explored potential cognitive effects. A 2025 phase-2 trial (Cury et al., 2025) tested a low-dose THC-CBD extract for 26 weeks in 28 AD patients. While placebo participants declined on the MMSE as expected, the treatment group showed a slight improvement, producing a 1.7-point difference at endpoint. No serious adverse events were reported, suggesting that low-dose combination formulations are generally well tolerated.
The strongest evidence to date comes from a trial evaluating dronabinol in 75 patients with severe AD (Johns Hopkins Medicine, 2024). Over three weeks, dronabinol reduced agitation by roughly 30% on the Pittsburgh Agitation Scale, whereas the placebo produced no improvement. Importantly, dronabinol’s calming effect was comparable to antipsychotics but occurred without major adverse effects like delirium or seizures. These results suggest that controlled synthetic THC formulations may offer a safer alternative for behavioural management in advanced AD.
4.5 Potential Therapeutic Strategies: Single vs Multi-Cannabinoid Approaches
Overall, cannabinoids influence AD through multiple pathways, including reducing amyloid and tau pathology, protecting neurons from oxidative stress, and modulating neuroinflammation and excitotoxicity. Single compounds like THC or CBD can provide benefits on their own. THC can help with pain and nausea but may cause anxiety or memory issues, whereas CBD exhibits neuroprotective and anti-inflammatory effects that require careful dose management.
Combining cannabinoids, especially THC and CBD, appears to offer a complementary approach. CBD can mitigate some of THC’s negative effects and, by acting on several receptors, engages multiple neuroprotective mechanisms simultaneously. Animal studies indicate that THC + CBD combinations improve memory and reduce Alzheimer’s-related changes more effectively than single compounds. The inclusion of minor cannabinoids may further enhance these effects, supporting the concept of the “entourage effect”.
When considering potential treatment strategies, factors such as age, CBD:THC ratio, and dose-response relationships are important to optimize efficacy and safety. While clinical evidence is still limited, these findings provide a framework for exploring multi-cannabinoid approaches in future research and therapeutic development.
5. Ethical, Cultural, and Wellness Considerations in the Use of Cannabinoids for Alzheimer’s Disease
Cannabinoids are increasingly being investigated for their ability to treat behavioral, psychological, and neuroinflammatory symptoms linked with Alzheimer’s disease. While much of the scientific discussion focuses on biological causes and clinical outcomes, incorporating cannabis-based medicines into dementia care presents complicated ethical, cultural, and wellness issues. These include cannabis’ long-standing spiritual and cultural significance, the growing wellness market and its regulatory gaps, issues with informed consent and surrogate decision-making in dementia, and structural inequities that influence who has access to cannabinoid-based treatment. Together, these factors show that the debate over cannabinoids and Alzheimer’s disease must go beyond pharmacology and include broader social and ethical dimensions.
5.1 Cultural and Spiritual Contexts of Cannabis Use
Cannabis has a long history in spiritual, ritualistic, and cultural traditions from different societies. Cannabis has long been utilized in numerous traditions, including Hinduism, Buddhism, different African ethnomedical practices, and Rastafarianism, to facilitate spiritual connection, healing, meditation, or ritual purification (Ferrara, 2022). These traditions view cannabis not as a recreational narcotic, but as a plant with symbolic, therapeutic, and holy meaning. The cultural significance of cannabis influences how families view and embrace cannabinoid-based dementia treatments.
Some communities may view cannabinoid therapy as congruent with traditional healing practices, contributing to acceptance of CBD or THC as “natural” or spiritually aligned treatments for an elder with Alzheimer’s. Ferrara (2022) notes that cannabis historically functioned as an entheogen, an agent used to stimulate introspection, relieving suffering, or fostering ritual wellness, meanings that exist in many diasporic and Indigenous groups today. In contrast, in cultures shaped by prohibition, criminalization, or religious restrictions, cannabis may be stigmatized or viewed negatively. According to Karki et al. (2022), cultural perceptions of cannabis have a strong influence on public attitudes toward its medical use, so clinicians must be culturally sensitive when discussing cannabinoid therapy with families.
The cultural framing of cannabis therefore connects with ethical care by influencing treatment acceptance, caregiver beliefs, and patient dignity. Culturally competent healthcare must recognize these various histories rather than assuming cannabis is either universally acceptable or universally banned.
5.2 Wellness Applications, Mislabeled Products, and Ethical Risks
The rapidly expanding CBD wellness sector adds another layer of ethical complication. Many caregivers use over-the-counter CBD oils, tinctures, and gummies marketed for sleep, anxiety, appetite stimulation, or general “brain health.” However, multiple studies show that these products particularly in the unregulated wellness market are frequently mislabeled or contaminated, posing a significant risk to older adults with cognitive impairment.
In a widely referenced JAMA study, Bonn-Miller et al. (2017) discovered that over 70% of online CBD products had incorrect CBD or THC concentrations, with 21% having unexpected quantities of THC. More recent research shows that the problem persists. Hopkins Medicine (2022) also documented “widespread mislabeling” of CBD concentration in retail items, while Drexel University researchers discovered that many hemp-derived CBD/THC products promoted as “non-psychoactive” actually contained enough THC to cause intoxication. A Colorado statewide audit revealed that cannabis flower products often exaggerated THC potency, and cannabidiol oils frequently displayed inconsistent or incorrect cannabinoid ratios (University of Colorado Boulder, 2025). A countrywide review in Canada also discovered “significant discrepancies” between labeled and real content on cannabis oil labeling (MJBizDaily, 2024).
Individuals with Alzheimer’s are medically vulnerable, very sensitive to psychoactive substances, and frequently take many drugs, meaning that utilizing incorrectly labeled or contaminated items poses major ethical concerns. Caregivers may mistakenly offer THC-containing medications to a cognitively challenged elderly person, increasing the risk of drowsiness, confusion, falls, and psychosis. The commercialization of CBD wellness culture has the potential to exploit vulnerable families, who may assume they are obtaining safe, natural treatments when the goods are not quality controlled. This conflicts with the ethical ideals of nonmaleficence, beneficence, and justice, particularly when marketing targets caregivers looking for hope in the face of a progressing, incurable sickness.
5.3 Autonomy, Informed Consent, and Surrogate Decision-Making
Alzheimer’s disease progressively impairs memory, communication, judgment, and decision-making abilities. As a result, the majority of patients getting cannabinoid-based therapy are unlikely to provide meaningful informed consent. This imposes an ethical responsibility on caregivers and surrogate decision-makers who must balance risks and rewards on behalf of their patients.
The ethics of consent in dementia care are widely documented. According to Al-Mokdad et al. (2025), people with Alzheimer’s disease are a highly vulnerable population who require additional protections to maintain their dignity, autonomy, and personhood. Hernández-Marrero (2021) adds that judging decision-making competence is often unclear, variable, and impacted by environmental context but it is crucial since cognitively handicapped people are more vulnerable to pressure or exploitation. Surrogates must avoid “therapeutic misconception” the belief that experimental treatments like cannabinoids provide guaranteed benefits (Wilkins, 2020).
In the context of cannabinoid therapy, ethical concerns arise when surrogates choose CBD or THC products without fully knowing dosage, side effects, or pharmacological interactions. According to Fox (2019), surrogate decision-making is even more problematic among socially marginalized or medically impoverished populations, where distrust of medical systems and limited access to professional supervision can lead to ineffective or hazardous treatment options.
Given these difficulties, clinicians should actively participate in shared decision-making with caregivers to ensure that marijuana usage is based on evidence, safety, and respect for the patient’s previously expressed values.
5.4 Equity, Stigma, and Structural Considerations
Cannabis carries unequal historical burdens. Its prohibition has disproportionately impacted racialized communities, shaping ongoing stigma. Older adults who lived through penalizing periods of cannabis criminalization may link cannabinoids with delinquency rather than medicine, impacting their acceptance of therapy. These differences hinder the ethical integration of cannabis treatments into dementia care.
Furthermore, pricing is a significant hurdle. High-quality, lab-tested cannabis medicines can be costly and rarely reimbursed by insurance, limiting access to richer households. As Bahji et al. (2019) emphasize in their review of cannabis for dementia-related neuropsychiatric symptoms, research involvement skewing toward higher-income groups perpetuates imbalances in knowledge generation. Justice requires that new medicines do not aggravate inequality in dementia care.
5.5 Future Directions
1. High-quality clinical trials.
The majority of studies on cannabis in dementia are small, diverse, and short-term. Systematic reviews indicate promising results for agitation, sleep, and hunger, but insufficient evidence for cognition or long-term safety (Liu et al., 2015; Stella et al., 2021; Outen et al., 2021). Recent randomized trials of dronabinol have shown promising reductions in agitation and aggression (Rosenberg et al., 2025), but bigger, geographically diversified phase III trials are required.
2. Development of safer, non-psychoactive cannabinoids
Future study should focus on minor cannabinoids (e.g., CBG, CBDV) that have anti-inflammatory or neuroprotective characteristics but have little euphoric effect. Formulations with stable ratios, slow-release methods, or microdosing procedures may improve tolerability in elderly individuals.
3. Standardization and strict regulation
Given the widespread evidence of mislabeling and varying product quality in commercially accessible marijuana medicines, there is an urgent need for strong regulation and standards to protect Alzheimer’s patients. Numerous studies have found that CBD and THC products frequently contain incorrect cannabinoid concentrations, unexpected levels of psychoactive compounds, or contamination with harmful substances such as pesticides and heavy metals (Bonn-Miller et al., 2017; Drexel University, 2022; Johns Hopkins Medicine, 2022). To ensure safety and dependability, regulatory agencies must demand batch-level laboratory testing, accurate and transparent CBD:THC ratio labeling, and routine screening for contaminants like as heavy metals, residual solvents, and agricultural pesticides. In addition, due to their increased susceptibility to psychoactive effects and frequent use of several drugs, older persons require clear, evidence-based dose guidelines. Strengthening these regulatory procedures is crucial for preventing harm and assuring the safety and ethical administration of cannabinoid-based therapies for Alzheimer’s disease.
4. Ethical frameworks for dementia-specific cannabis use
Policies guiding the use of cannabinoids in Alzheimer’s care must promote patient safety, autonomy, and ethical compliance. This includes adopting standardized consent processes that specify how to assess decision-making capacity and when surrogate decision-makers should be involved. Caregiver education programs are also necessary to ensure that families completely grasp the dosing, potential interactions, expected benefits, and hazards involved with cannabis usage. Furthermore, clear measures must be implemented to prevent cannabis from being used as a kind of pharmacological restriction, especially considering the vulnerability of dementia patients and the ethical considerations surrounding sedation for convenience rather than care. Finally, robust monitoring systems for documenting and responding to adverse effects are necessary to ensure ongoing patient safety and to build reliable data that can inform future clinical guidelines. Together, these regulations establish an ethical framework that promotes responsible, transparent, and patient-centered cannabinoid usage in dementia care.
5. Integration of Cultural Competence
Clinicians must acknowledge that cannabis has various cultural implications. Integrating cultural and spiritual aspects into treatment boosts trust, communication, and ethical integrity.
Conclusion
Cannabinoids represent a promising but still developing area of Alzheimer’s disease research. Across mechanistic, preclinical, and clinical studies, these compounds demonstrate activity on multiple pathways implicated in AD, including amyloid-β aggregation, tau hyperphosphorylation, neuroinflammation, excitotoxicity, and oxidative stress. This multi-target profile distinguishes cannabinoids from current AD treatments, which generally provide limited symptomatic relief and minimal disease modification.
Preclinical studies consistently show that THC, CBD, and especially THC + CBD combinations improve synaptic function, modulate microglial activation, and support memory performance in AD models. Human research remains limited but suggests potential benefits for behavioural symptoms such as agitation, with synthetic cannabinoids like nabilone and dronabinol demonstrating measurable reductions in neuropsychiatric distress. Emerging clinical findings also indicate that balanced low-dose cannabis extracts may help stabilize or modestly improve cognitive scores.
However, these therapeutic possibilities must be evaluated alongside ethical considerations. Alzheimer’s patients face challenges in providing informed consent, and psychoactive or sedative effects may complicate treatment decisions for caregivers and clinicians. Issues of patient vulnerability, safety, and responsible administration must be central to any future application of cannabinoid-based therapies.
Future research should emphasize controlled dosing, standardized formulations, optimized cannabinoid ratios, long-term safety assessments, and the potential role of minor cannabinoids. While cannabinoids are not a cure for Alzheimer’s disease, the evidence demonstrates meaningful therapeutic potential that warrants continued, ethically guided investigation. Cannabinoids may ultimately contribute to a broader, more holistic approach to AD treatment that integrates neuroprotection, symptom management, and improved quality of life for patients and caregivers.
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