CBG and Neuroinflammation: What a 2018 Study Found

Important: This article is an educational overview of preclinical research. The study discussed used a mouse model — not human subjects. The findings do not establish that CBG treats, prevents, or slows any neurodegenerative disease in humans. CBG products are food supplements, not medicines. Always consult a qualified healthcare provider for any concerns about neurological health.

Neuroinflammation — chronic inflammation within the brain — plays a central role in the development and progression of neurodegenerative diseases such as Parkinson’s and Alzheimer’s. Researchers actively explore compounds that might modulate this process. Among these, CBG (cannabigerol) has attracted growing scientific interest.

A 2018 study published in the International Journal of Molecular Sciences investigated CBG’s effects on neuroinflammation using a mouse model. This article explains what the researchers did, what they found, and — importantly — what their findings do and do not tell us about CBG’s potential relevance to human neurodegenerative conditions.

This is an overview of early-stage, preclinical research. Mouse models are a valuable and necessary step. However, findings in animal models do not automatically translate to human outcomes. That distinction matters when the topic involves serious conditions like Parkinson’s and Alzheimer’s.

What Is Neuroinflammation?

Neuroinflammation refers to inflammation within the central nervous system — the brain and spinal cord. It is a natural immune response that becomes problematic when it turns chronic. Persistent neuroinflammation contributes to progressive neuronal loss in neurodegenerative diseases.

In Parkinson’s disease, researchers observe neuroinflammation alongside the degeneration of dopaminergic neurons — the neurons responsible for producing dopamine. In Alzheimer’s disease, neuroinflammation occurs alongside amyloid-beta plaques and neurofibrillary tangles. In both conditions, the inflammatory environment appears to accelerate neuronal damage.

Oxidative stress is closely related to neuroinflammation. It results from an imbalance between free radical production and the body’s antioxidant defences. Because neurons are particularly vulnerable to oxidative damage, compounds with antioxidant properties attract research interest in this context.

What Is CBG?

CBG stands for cannabigerol. It is a non-intoxicating cannabinoid from the hemp plant — often called the mother cannabinoid because the plant produces it first, before converting it into CBD, THC, and others as it matures.

CBG interacts with the endocannabinoid system (ECS), including both CB1 and CB2 receptors. CB2 receptors concentrate in immune tissue and play a role in regulating inflammation. Because of this, researchers study CBG in inflammatory contexts — including neuroinflammation.

In addition to cannabinoid receptor activity, preclinical research has examined CBG for antioxidant properties. However, most of this research is in cell cultures or animal models. Human clinical trials on CBG for any condition remain very limited.

The 2018 Study: What Researchers Did

The study by Rodríguez-Cueto et al. investigated CBG’s effects on neuroinflammation using a validated mouse model designed to mimic aspects of human neuroinflammatory conditions.

Researchers administered CBG to the mice and then measured a range of biomarkers associated with inflammation and oxidative stress — specifically inflammatory cytokines and markers of oxidative stress in brain tissue. The mouse model was validated against known features of neuroinflammatory disease, so the research design was scientifically sound for its stage.

The key question is what the findings mean and how far they can be extrapolated toward human conditions.

What the Study Found

Effects on Inflammatory Markers

In the mouse model, CBG appeared to inhibit the release of pro-inflammatory cytokines — the proteins that drive the brain’s inflammatory response. Researchers found a reduction in these markers following CBG administration, suggesting that CBG modulated the neuroinflammatory response in this animal model.

This is scientifically interesting because excessive cytokine release is a feature of both Parkinson’s and Alzheimer’s pathology. However, demonstrating cytokine reduction in mice does not establish the same effect in humans, or that it would be clinically meaningful if it did.

Effects on Oxidative Stress Markers

The study also found that CBG demonstrated antioxidant activity in mouse brain tissue. Oxidative stress markers were lower in CBG-treated animals than in controls. Because oxidative damage contributes significantly to neuronal loss in neurodegenerative conditions, the researchers considered this worth further investigation.

Again, antioxidant effects in a mouse model do not directly translate to neuroprotective effects in humans. The metabolic and biological differences between mice and humans mean that promising preclinical results frequently do not replicate in clinical trials.

Relevance to Parkinson’s and Alzheimer’s Research

The study’s authors discussed the potential relevance of their findings to Parkinson’s and Alzheimer’s — both of which involve chronic neuroinflammation and oxidative stress. Because CBG reduced both in the mouse model, they proposed it as a candidate worth studying further in these disease contexts.

However, it is important to be precise: the 2018 study was not a Parkinson’s study or an Alzheimer’s study. It used a general neuroinflammation model. The connection to these specific diseases is a research hypothesis — not a finding in itself.

The step from a mouse neuroinflammation study to a clinical intervention for Parkinson’s or Alzheimer’s involves many further research stages, each of which can fail. So the findings are a starting point for further investigation, not evidence of therapeutic benefit in humans.

Why This Research Direction Matters

Despite the limitations of a single mouse study, the research direction is worth understanding. Neuroinflammation is increasingly recognised as a therapeutic target in neurodegenerative disease. Current approved treatments for both Parkinson’s and Alzheimer’s have significant limitations and do not halt disease progression.

Because of this treatment gap, researchers explore a wide range of compounds with anti-inflammatory and antioxidant properties. CBG is one of several candidates in this space. Its non-intoxicating nature and apparent safety profile make it a reasonable subject of study — but one early candidate among many, not a proven treatment.

The 2018 study contributes to a body of preclinical literature that researchers use to decide which compounds warrant further investigation. For CBG in neuroinflammation, the next step would be human safety trials, followed by efficacy trials in relevant patient populations. Those trials do not yet exist.

Final Thoughts

The 2018 study found that CBG reduced neuroinflammation and oxidative stress markers in a mouse model. The methodology was sound for its stage, and the findings generated reasonable scientific interest in CBG as a candidate for further study.

However, this is one preclinical study. It establishes a hypothesis worth testing — not a therapeutic benefit. The gap between a positive mouse model result and a clinically useful treatment is large, and most candidates do not make it across.

For people living with Parkinson’s or Alzheimer’s, or caring for someone who is: this research is not actionable as a treatment decision. CBG products are food supplements, not medicines. If you want to discuss cannabinoids in the context of a neurological condition, speak to a neurologist or specialist who knows your specific situation.

Disclaimer: This blog is for informational and educational purposes only. We review and reference available studies and reputable sources; however, content may not reflect the most current research or regulations and should not be taken as medical, legal, or professional advice. We do not make or imply health claims. Products mentioned are not intended to diagnose, treat, cure, or prevent any disease and statements have not been evaluated by EFSA or the FDA. Effects can vary between individuals. Always consult a qualified healthcare professional before use and verify that any product or ingredient is lawful in your jurisdiction.