Studies Show CBD Protects Brain From Alzheimer’s

CBD acts as an anti-inflammatory and neuroprotectant with the strong potential to prevent neuronal damage.

Alzheimer’s disease (AD) is the most common form of dementia affecting over 33 million people worldwide. Alarmingly, this number is expected to reach 115 million by year 2050. In the beginning stages, AD typically manifests as a mild loss of short term memory, spatial disorientation and communication difficulties. It later progresses to severe disruptions in cognitive ability, impairments in speech and facial recognition. AD patients are also susceptible to illness encompassing other organ systems.

CBD Is a Potent Anti-Inflammatory in Neurological Tissue

The available FDA-approved AD treatments alleviate the symptoms rather than treat the underlying pathology. However, new avenues of cannabinoid therapeutics have opened up recently. We already reported the work that was done using THC as a promising therapy for AD. Here, we will summarize the aspects of CBD that make it an attractive candidate for developing new therapeutics for AD.

As a neuroprotective agent, CBD is a prime candidate for new treatment strategies. In studies conducted over the past decade, it demonstrated strong potential to prevent degeneration of the brain centers crucial for cognition and integration (hippocampus and cortex). It also has anti-inflammatory and anti-oxidant properties.

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Importantly, CBD also regulates cell migration of microglia, which are resident immune cells of the brain. Furthermore, CBD reduced production of toxic neurofibrillary tangles and plaques, thus improving neuronal cell viability. Alzheimer’s involves all of the above complex pathological changes in the brain. CBD is the perfect therapeutic agent because it has the potential to affect many of these aspects.

Studies in Rodent Models of AD

Several studies show the effects of medicine on mice with the disease state (of Alzheimer’s) artificially created. Fibrillar Ab peptides are the hallmark of  AD in humans, so these are injected into the mouse to accomplish this.

Researchers injected the human Ab directly into the hippocampus of rodent eubjects, followed by daily intraperitoneal injections of CBD (2.5 or 10mg/kg) for 7 days. This treatment reduces neuroinflammation and consequently neuronal damage.

These effects have been hypothesized to occur due to CBD’s ability to act as an inverse agonist of CB2 receptors. This means that it binds to receptor sites of other molecules (like THC) and prevents these from binding. Studies conducted in a rat model of AD revealed that the anti-inflammatory and neuroprotective effects may also be conferred through its interactions with PPARg receptors. When rats injected with Ab were administered CBD at 10mg/kg, alongside PPARg antagonist, for 15 days, the neuroinflammatory program of gene expression was initiated.

Conversely, rats given only CBD without the antagonism of PPARg receptors, the inflammatory gene expression pathways were significantly downregulated, thus preventing gliosis (inflammation). Most importantly, this study found that the protection of CBD resulted in the rodent maintaining neuron structures to a level similar to that observed in non-AD control rats.

Collectively, these results imply that, even after the onset of AD and in the presence of Ab plaques, administration of CBD could reverse that. Brain centers for learning, memory, and cognition may be completely protected from timely CBD administration.

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Other Models of AD for Future CBD Therapeutic Research

A research group from Puerto Rico demonstrated their newest data at the Experimental Biology Conference in April 2019. The objective was to test the therapeutic potential of CBD oil in alleviating the symptoms of AD. Worms, or C. elegans, act as the animal model for many experiments.  This allows researchers a first look at how a molecule operates in a simple animal body.

The scientists found that exposure to CBD oil for 24 hours reduced locomotor deficits that AD worms displayed. Furthermore, CBD-treated worms demonstrated improvement in short-term associative memory compared to the untreated counterparts, albeit without statistical significance. Since this was just a pilot study, the scientists are working on increasing the sample size. A larger sample would give better indication whether such improvements in memory are indeed occurring.


The collected data provides “proof of principle.” This means there is justification for exploring CBD therapy for this disease.

Proper dosing, and how that translates to humans, are two questions that need to be answered. We would like to see demonstration of similar protective effects in animals representing age at which AD strikes humans. Finally, the potential for increasing efficacy if THC and CBD were administered together needs to be explored.


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