The scientists from Israel and Spain say cannabis-based treatments could improve memory loss in Alzheimer's sufferers.
The revelation was made this week at a symposium of cannabis experts hosted by the Royal Pharmaceutical Society of Great Britain (RPSGB) where the scientists said that a compound present in cannabis significantly slows memory problems caused by the disease.
Ten years ago the RPSGB launched its protocols to demonstrate the therapeutic effectiveness of cannabis which led to Government-funded trials in Britain to explore the benefits for patients with multiple sclerosis and in the treatment of severe pain.
Cannabis-derived medicines have subsequently entered the market and are currently available to patients in Canada.
The claim follows successful tests in mice and the scientists are now calling for funding for trials to be conducted in humans.
Cannabis is thought to trigger harmful mind-altering effects in some people but the scientists say the medicinal compound in question, cannabidiol, is not a hallucinogenic ingredient.
Professor Raphael Mechoulam from the Hebrew University of Jerusalem, also found that the symptoms of type 1 diabetes can be helped by cannabidiol.
Professor Mechoulam however warns against the use of cannabis by Alzheimer's patients because the psychoactive ingredient Tetrahydrocannabinol (THC) could have damaging effects on memory.
Experts are calling for clinical trials into the potential benefits of the non-psychoactive components of cannabis and they too stress that such treatments are not the same as recreational cannabis use.
Professor Tony Moffat, chairman of the Symposium says progress has been made in the last ten years but more research is needed as there is considerable interest in the medical benefits of cannabis and related compounds for a range of conditions including arthritis, multiple sclerosis and neurological pain.
Alzheimer's disease is the commonest form of dementia, which affects an estimated 24.3 million people worldwide.
We now have published that, even earlier in the development of diabetes, people who are not yet insulin resistant show a low secretion of PYY. They have a blunted post-meal secretion of this hormone, making them less likely to feel satiety, and more likely to gain weight.
Professor Campbell's research involved elaborate testing of two groups of people, eight in each group, over a period of two years. One group had relatives with Type 2 diabetes, the other group had no family history of the disease. The groups were matched for gender, for age and for adiposity.
It was most important to match the groups for their fatness, said Professor Campbell. The only difference was their relatives. You assume that they are carrying the genetic burden of diabetes, which we already know to be a reality.
Low levels of PYY at this very early pre-diabetes stage could be used as a marker, or predictor, that Type 2 diabetes is very likely to develop.
As a clinician, I am hopeful that it will be possible to screen extensively in the future, and therefore stem the spread of this debilitating disease.
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