IIn recent years, Ozempic has become a totem for weight loss. About 1 in 8 adults Reports say he took the popular diabetes and weight loss drug, chemically known as semaglutide, at some point.1 Semiglutide is Glucagon-like peptide-1 (GLP-1) mimetics It stimulates insulin production, slowing stomach emptying and making you feel fuller for longer.2 Researchers have been studying this molecule for more than 20 years and are understanding how it finely regulates metabolism. But scientists are now discovering that the drug has other far-reaching but less-explained effects on the brain. New research presented at the October 2024 Society for Neuroscience meeting shows that semiglutamide can alleviate cognitive impairment associated with Alzheimer’s disease, reduce acute and chronic pain, and alter motivation to exercise in rodent models. reported the scientists.
“The brain is the organ that controls what you eat, how you eat, and how much energy you expend,” he said. Karolina Skibickais a neuroscientist at Pennsylvania State University and an expert on GLP-1, but was not involved in the study. So it makes sense that drugs that regulate appetite would also affect the brain. However, it turns out that semaglutide is also involved in physiological processes far removed from metabolism.
Previously, researchers showed that GLP-1 mimics can alter the associated reward value. food, alcohol, cocaineand nicotine.3～6 When they administered GLP-1 or its analogs to rodents, they observed a decrease in their willingness to obtain these substances.ralph dileoneNeuroscientists at Yale University were interested in understanding whether this effect could lead to motivation to exercise, especially since mice are naturally drawn to exercise and see it as a reward. “If you give these rats wheels, they’ll run anywhere between 10 to 12 kilometers every night,” DiLeone says. He showed that giving semaglutide to mice reduced their desire to run, regardless of how much they ate. A decrease in running time corresponds to a lack of interest in exercise.
The brain also perceives rewards in other ways, such as eating food. This plays an important role in pain relief, a phenomenon called ingestive analgesia. “In my experience, when you’re sick, eating makes you feel a little bit better,” he said. Kim Young Hoa pain researcher at Kasen University. Considering that GLP-1 levels increase after eating, Kim investigated whether and how this peptide could modulate pain caused by various factors. An important receptor for transmitting pain is the transient receptor potential vanilloid 1 (TRPV1) channel. In chronic pain, not only are TRPV1 levels increased in pain-sensing neurons, but the receptors also become hypersensitive to stimuli. Dr. Kim showed that treating mice with semaglutide reduced their sensitivity to painful stimuli, such as heat, compared to control mice. He also reported that semaglutide reduced pain in both acute and chronic pain models.
Another therapeutic avenue for semaglutide is in the fight against neurodegenerative diseases. Chronically high levels of blood sugar can cause inflammation, neuron death, brain aging, cognitive impairment, and even dementia. Researchers have shown that GLP-1 works by: Relationship between metabolic disorders and brain disorders.7 In recent research, Emile AndrianberozonNeuroscientists at Neurofit have shown that semaglutide can improve memory impairment in a mouse model of late-stage Alzheimer’s disease. The accumulation of misfolded amyloid-beta protein and the resulting inflammation in the brain causes Alzheimer’s disease. Andrian Belloson and his team found that administering semaglutide for one week to mice suffering from these protein plaques, or inflammation, significantly improved memory and cognitive deficits compared to mice given a placebo. It was confirmed that Inflammation also causes neuron death, a hallmark of Alzheimer’s disease. The research team noted that semaglutide protected these neurons and prevented their death.
These new findings have laid the foundation for investigating the widespread GLP-1 cast in the body. “We certainly don’t know everything,” Skibicka says. “We have the following populations. [GLP-1] A receptor we never asked what it does. They might be doing something amazing. ” Regarding what we know about how GLP-1 orchestrates these diverse behaviors, DiLeone says there may be common underlying pathways, but these It is likely that there are unique factors that promote this effect. This opens up the possibility of targeting them, especially at the behavioral and therapeutic level.
