Researchers from the Universities of Bonn and Mainz have now discovered a hitherto unknown function of the cannabinoid-1 receptor (CB1). A receptor is a protein that can bind to other substances, triggering a chain of signals. Cannabinoids such as THC – the active agent in cannabis sativa – and endocannabinoids formed by the body bind to the CB1 receptors. The existence of this receptor is also the reason for the intoxicating effect of hashish and marijuana.
Not only does the CB1 receptor have an addictive potential, but it also plays a role in the degeneration of the brain. “If we switch off the receptor using gene technology, mouse brains age much faster,” said Önder Albayram, principal author of the publication and a doctoral student on the team of Professor Andreas Zimmer from the Institut für Molekulare Psychiatrie at the University of Bonn. “This means that the CB1 signal system has a protective effect for nerve cells.”
The animals in which the CB1 receptor had been switched off (the knock-out mice) clearly differed from their kind. “The knock-out mice showed clearly diminished learning and memory capacity,” said Associate Professor Doctor Andras Bilkei-Gorzo from Professor Zimmer’s team, who led the study. “In addition, they showed a clear loss of nerve cells in the hippocampus,” he explained further. This part of the brain is the central area for forming and storing information. In addition, the researchers found inflammation processes in the brain. As the mice advanced in age, the degenerative processes became increasingly noticeable.
The animals with the intact CB1 receptor, to the contrary, did clearly better with regard to their learning and memory capabilities, as well as the health of their nerve cells. “The root cause of aging is one of the secrets of life,” commented Albayram. This study has begun to open the door to solving this enigma. The processes in the mouse brains have a surprising number of parallels with age-related changes in human brains. So, the endocannabinoid system may also present a protective mechanism in the aging of the human brain.
MEDICA.de; Source: University of Bonn