A preclinical study found that repeated CBG treatment prevented a long-term recognition memory impairment induced by MK-801 in male rats, an experimental model used to study cognitive deficits relevant to schizophrenia. The effect did not appear to involve restoring reduced BDNF protein levels, though changes in TrkB messenger RNA point to a possible mechanism that will require further research.

CBG (cannabigerol), the precursor molecule from which THC and CBD are formed in the cannabis plant, and a cannabinoid far less studied than either of them, has just given researchers another reason to pay attention.

A preclinical study published online ahead of print by Pharmacology Biochemistry and Behavior found that CBG prevented a long-term memory deficit in male rats treated with MK-801, a compound commonly used in experimental models of cognitive impairments associated with schizophrenia.

Does that mean CBG improves memory in people with schizophrenia? No, but the results offer an interesting clue about a problem for which there are still no approved treatments: the cognitive deficits that can accompany the disorder.

CBG and a Memory Problem

Schizophrenia affects about 23 million people worldwide, or roughly one in 345, according to the World Health Organization, and can cause persistent difficulties across a range of cognitive functions.

These impairments can affect memory, attention, learning and executive function, and can have real-world consequences for a person’s ability to study, work, maintain relationships or live independently. The authors of the new study describe the pharmacological options for treating them as limited, note that some research finds all antipsychotics have minimal effect on cognitive function, and cite estimates that 30% to 35% of patients with schizophrenia are treatment-resistant.

That’s where the new study comes in. It was carried out by researchers at the Instituto de Investigaciones Biológicas Clemente Estable and the Universidad de la República, in Uruguay, together with colleagues at Phytoplant Research, the Universitat de Vic-Universitat Central de Catalunya, the University of Barcelona and Spain’s Biomedical Research Networking Center in Mental Health.

To study CBG’s potential effects, the researchers used MK-801, a substance that blocks certain NMDA receptors in the brain. In animals, this compound can cause cognitive impairments that mimic some of the deficits observed in schizophrenia, which is why it is commonly used as an experimental model.

The study used 67 adult male Wistar rats, bred and housed at the institute’s facilities in Montevideo. The researchers gave them repeated doses of CBG at 10 mg/kg, and some of the animals then received a single 0.1 mg/kg dose of MK-801, while others received a control solution. Then came the test.

Did the Rats Remember What They Had Seen?

To measure memory, the researchers used a fairly intuitive test known as novel object recognition.

First, the rats are exposed to certain objects. The following day, one of them is replaced with a new one.

Normally, if an animal remembers what it saw before, it spends more time exploring the new object. If it fails to distinguish between the old and new objects, that may indicate impaired recognition memory.

That is exactly what happened in the rats that received only MK-801: they stopped showing a preference for the new object.

By contrast, the rats that had received CBG retained that ability, even after receiving MK-801.

According to the authors, CBG prevented the long-term recognition memory impairment caused by the experimental compound.

The researchers also had to rule out a much less exciting explanation: that the treated rats were simply moving around more and therefore spent more time exploring. According to the study, neither MK-801 nor CBG nor the combination affected locomotor activity. MK-801 did reduce rearing, the behavior of standing up on the hind legs, but the authors report that this did not change how long the animals spent exploring the objects.

Things Got a Little Stranger Inside the Brain

The researchers also tried to determine how that effect might be occurring.

One of the main suspects was BDNF, a protein associated with brain plasticity, learning and memory.

MK-801 reduced BDNF protein levels in two regions involved in these processes: the hippocampus and the medial prefrontal cortex. If CBG was preventing the cognitive impairment, one logical possibility was that it might also restore those BDNF levels. But it didn’t.

Even though the rats maintained their performance on the memory test, CBG did not restore the BDNF protein levels reduced by MK-801.

Then another clue emerged: the combination of CBG and MK-801 significantly increased messenger RNA expression for TrkB, a receptor closely involved in BDNF signaling, in the medial prefrontal cortex.

In very simplified terms, CBG appeared to influence part of the molecular machinery involved in memory, but not through the most obvious mechanism the researchers expected to find.

The authors suggest that TrkB signaling may contribute to the observed effect through a mechanism independent of direct changes in BDNF.

Promising, Yes; a Treatment, Not Yet

The study was conducted exclusively in male rats. The researchers did not test different CBG doses or dosing schedules, and they have not yet confirmed whether the changes observed in TrkB messenger RNA extend to the protein level.

Also, MK-801 does not give rats “schizophrenia.” It is an experimental tool that mimics certain cognitive deficits relevant to the study of specific aspects of the disorder.

For that reason, the results do not show that CBG treats schizophrenia, improves memory in human patients or should be used clinically for that purpose.

What they do show is something much narrower and, for that very reason, still interesting: in this preclinical model, CBG was able to preserve a form of memory that MK-801 had impaired.

And for a cannabinoid that remains far less studied than its more famous relatives, that is enough to justify a second look.

Disclosure: the study was funded by Uruguayan public science programs, including MEC-DICYT and PEDECIBA. The cannabigerol was donated by Phytoplant Research S.L.U., a Spanish cannabis research company, and two of the paper’s authors, Carlos Ferreiro-Vera and Verónica Sánchez de Medina, work for the company, according to its competing interest declaration.

Editor’s note: this article describes findings in animals. Preclinical research is an early step and does not establish that a compound is safe or effective in people. Nothing here is medical advice, and no one should change or stop a prescribed treatment based on it.

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Labour MP and long-time medical cannabis advocate, Tonia Antoniazzi, has called on the government to fund a new observational trial to support children with drug-resistant epilepsy, who are still unable to access medical cannabis on the NHS.

Antoniazzi is spearheading a new campaign launched in memory of Hannah Deacon, the mother of Alfie Dingley, who campaigned for the legalisation of medical cannabis in 2018. Hannah died of cancer last year, aged just 45. 

Her high-profile campaign led to Alfie, who has a rare and severe form of treatment-resistant epilepsy, becoming the first person to obtain a full licence for the prescription of medical cannabis through the NHS in June 2018.

Later that year, on 1 November, the government announced the rescheduling of cannabis-based medicines, making them legal to prescribe by doctors on the specialist register. 

Almost eight years on, an estimated 80,000 patients are now able to access medical cannabis through private clinics in the UK, but only four children (including Alfie) receive prescriptions through the NHS, whilst other families face costs of around £15,000 per year.

Hannah Deacon died last year after a short battle with cancer.

An “unacceptable burden”

During Prime Minister’s Questions on Wednesday, 4th March, Antoniazzi, MP for Gower, asked Keir Starmer to commit a “modest” £2 million for an observational trial to relieve these families of this “unacceptable burden”. 

“Many families are still paying around £1,300 a month for a treatment that is already legal to prescribe,” said Antoniazzi, who has previously accompanied families travelling to the Netherlands to access medical cannabis.

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The proposed study would run alongside two previously announced NHS-funded randomised control trials (RCTs) on medical cannabis and epilepsy, which are being conducted by researchers at UCL. It would allow children who are currently prescribed the treatment privately to continue accessing it at no cost, while real-world data is collected.

The research team is said to have confirmed that an accompanying observational trial would be a viable option. However, the Prime Minister failed to commit to the additional funding, instead pointing to the £8 million already invested in RCTs. 

“Hannah Deacon’s campaign for her son, Alfie, was remarkable, and I know how much she’s missed,” Starmer told the House.

“We are investing £8 million in clinical trials on cannabis based medicines for conditions like drug-resistant epilepsy, and I want to see patients accessing safe, effective medicines and new treatments as quickly as possible.” 

The RCTs were first promised in 2019 following a review commissioned by former Health Secretary Matt Hancock. Although finally announced in 2024, they have since been delayed again.

Campaigners warn that these will take several years to complete and are not suitable for those children already prescribed medical cannabis, for whom the treatment has already significantly reduced seizures, where all other options have failed. 

“While I understand the government’s reticence to move towards any kind of drug reform… this is a titrated drug, and is widely accepted in other countries around the world,” Antoniazzi tells Cannabis Health.

“Why we are making it difficult for these families to access a prescription that makes their children’s lives so much easier baffles me.”

“We made her a promise we wouldn’t give up”

Even after Alfie secured his NHS prescription, Hannah continued campaigning to ensure other families could access the same treatment. Now, Antoniazzi and other parents say they will continue that fight in Hannah’s name.

“What drives me is Hannah, and how she fought for all families and how she fought for their children,” she adds.

“She was a really special woman, and her family wants her legacy to remain.”

In a post on her Instagram, Emma Appleby, who campaigned alongside Hannah on behalf of her daughter Teagan, said: “Although Hannah’s son had an NHS prescription, she continued to fight and stand alongside other families like mine who still had to battle… We all made a promise that we wouldn’t give up.”

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Medcan Family Foundation commented: “Hannah was a tireless advocate and a driving force behind progress for families fighting for access. She refused to accept a system that left children waiting without answers… Her legacy continues in this new campaign.”

You can support the Hannah Deacon Campaign for Access to Medical Cannabis by emailing your MP and signing Hannah’s petition here.

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