Old mice given THC, the active ingredient in marijuana, did better on learning and memory tests — though young mice did worse. It’s too early to say if this applies to humans, but the findings do shed some light into the possible effects of the drug.
Marijuana is known to have pain-relieving effects. People also think it might be bad for cognitive function, but there hasn’t been a lot of reliable research in this area. In an study published in Nature Medicine, researchers implanted young, full-grown, and old mice with little pumps that released tetrahydrocannabinol (THC) into them every day.
The scientists then gave the mice various learning and memory tests. Young mice given the THC did worse, but the old ones did better.
THC is one of the key components of cannabis; the chemical interacts with the numerous cannabinoid receptors in the central nervous system. In today’s study, all the mice (young, full-grown, and old) received low doses of THC via the pump for 28 days. After 33 days — so, after the mice were no longer getting the THC — scientists gave the mice the Morris water maze test, where mice have to escape a round pool by finding a platform that helps it escape.
In the control group, the older mice did worse than the young mice, which makes sense. The interesting part is that young mice given THC did worse than the control group. And older mice given THC did better than the control group. In fact, they did as well as the young mice in the control group.
These are very early results which should be taken with a grain of salt. Next, the team will do more investigations to learn more about the cause of these results, and try these experiments in other animals to see if the findings hold up.
Andreas Zimmer at the University of Bonn, Germany, and his colleagues studied mice aged 2 months (young), 12 months (mature) and 18 months (old). They implanted mini-pumps under the mice’s skin, and for 28 days these released either low doses of marijuana’s main active compound, delta-9 tetrahydrocannabinol (THC), or a solution without the drug.
After this period, the THC-treated mature and old mice performed as well as untreated young animals in memory and learning tests, whereas THC-treated young mice performed considerably worse.
In the brains of the treated mature and old mice, the structures of neuronal connections, or synapses, also reverted to those seen in untreated young animals, as did patterns of gene expression.
All of these changes depended on the function of a brain receptor that binds certain neurotransmitters as well as THC.
"The balance between detrimental, pro-aging, often stochastic processes and counteracting homeostatic mechanisms largely determines the progression of aging.
There is substantial evidence suggesting that the endocannabinoid system (ECS) is part of the latter system because it modulates the physiological processes underlying aging.
The activity of the ECS declines during aging, as CB1 receptor expression and coupling to G proteins are reduced in the brain tissues of older animals and the levels of the major endocannabinoid 2-arachidonoylglycerol (2-AG) are lower.
However, a direct link between endocannabinoid tone and aging symptoms has not been demonstrated. Here we show that a low dose of Δ9-tetrahydrocannabinol (THC) reversed the age-related decline in cognitive performance of mice aged 12 and 18 months. This behavioral effect was accompanied by enhanced expression of synaptic marker proteins and increased hippocampal spine density.
THC treatment restored hippocampal gene transcription patterns such that the expression profiles of THC-treated mice aged 12 months closely resembled those of THC-free animals aged 2 months.
The transcriptional effects of THC were critically dependent on glutamatergic CB1 receptors and histone acetylation, as their inhibition blocked the beneficial effects of THC. Thus, restoration of CB1 signaling in old individuals could be an effective strategy to treat age-related cognitive impairments."