Research
The genetically modified protein that can enhance memory

The engineered protein is activated by the drug rapamycin, which is known to increase life expectancy in preclinical models.
Scientists have genetically modified a brain molecule called LIMK1 to boost memory. The research team added a “molecular switch” to the protein which can be activated by administering a drug, rapamycin, known for its several anti-ageing effects on the brain.
The immunosuppressive drug is known to increase life expectancy and for its beneficial effects on the brain in preclinical models.
Marrying genetics and chemistry, the authors of the study describe this approach as “chemogenetic”.
Cristian Ripoli, associate professor of physiology at the Catholic University and first author of the study said: “In animals with age-related cognitive decline, using this gene therapy to modify the LIMK1 protein and activate it with the drug resulted in a significant memory improvement.
“This approach allows us to manipulate synaptic plasticity processes and memory in physiological and pathological conditions. Furthermore, it paves the way for the development of further ‘engineered’ proteins that could revolutionize research and therapy in the field of neurology,” the expert emphasizes.
Aside from improving scientific understanding of memory function, the research has unlocked potential applications in treating neuropsychiatric diseases like dementia.
The team consisted of neuroscientists from the Faculty of Medicine and Surgery of the Catholic University, Rome and the Fondazione Policlinico Universitario Agostino Gemelli IRCCS. The study was coordinated by Claudio Grassi, full professor of Physiology and Director of the Department of Neuroscience.
“Memory is a complex process that involves modifications in synapses, which are the connections between neurons, in specific brain areas such as the hippocampus, which is a neural structure playing a critical role in memory formation,” Grassi said.
“This phenomenon, known as synaptic plasticity, involves changes in the structure and function of synapses that occur when a neural circuit is activated, for example, by sensory experiences. These experiences promote the activation of complex signaling pathways involving numerous proteins”
The LIMK1 protein plays a crucial role in determining structural changes in neurons, namely the formation of dendritic spines, which enhance information transmission in neural networks and are crucial in learning and memory processes.
“Some of these proteins are particularly important for memory, in fact, reduced expression or modifications of these proteins are associated with alterations in cognitive functions,” Professor Grassi added.
“One of these proteins is LIMK1. The goal of our study was to regulate the activity of this protein, as it plays a key role in the maturation of dendritic spines between neurons. Controlling LIMK1 with a drug means being able to promote synaptic plasticity and, therefore, the physiological processes that depend on it.”
“The next step will be to verify the effectiveness of this treatment in experimental models of neurodegenerative diseases exhibiting memory deficits, such as Alzheimer’s disease. Further studies will also be necessary to validate the use of this technology in humans.”
The research was supported by the Italian Ministry of Education, University and Research, the American Alzheimer’s Association Foundation, and the Italian Ministry of Health,
News
Low doses of weight loss drugs may slow ageing

Microdoses of weight loss drugs like Ozempic could slow ageing and increase longevity, according to new research in mice.
The study found that exenatide, a drug with similar chemical make-up to Ozempic, produced molecular changes in mice that opposed typical patterns seen with ageing across multiple organs.
Scientists treated mice starting at 11 months of age with small doses of the drug for about 30 weeks, then compared tissue samples from brain, liver, kidney, muscle and fat.
Researchers from the Chinese University of Hong Kong measured levels of RNA and DNA modifications, proteins and metabolism-related molecules to assess how age-related molecular signatures had changed in each tissue.
The treated mice showed metabolic health consistent with younger animals, with their molecular “age-signature” significantly shifted to a younger-looking profile compared with untreated older mice.
Many of the drug’s positive effects appeared to involve brain activity, suggesting the brain acted as a hub influencing the ageing profiles of multiple organs throughout the body.
Exenatide and semaglutide (sold as Ozempic and Wegovy) are GLP-1 receptor agonists. These medicines mimic a naturally occurring hormone in the gut and brain that regulates appetite, helping people feel fuller for longer.
Originally developed for diabetes treatment, these drugs have surged in popularity for weight loss. A new trend has emerged online with some people reportedly taking very small doses for longevity, though health experts warn the anti-ageing effect has not been proven in humans.
“Our work has provided multifaceted evidence for a comprehensive body-wide anti-ageing strategy,” the researchers wrote. “Future longitudinal studies are necessary to explore whether GLP-1R agonism may complement other anti-ageing methods.”
The study examined multiple biological markers of ageing, including epigenetic modifications (changes to DNA that affect gene activity without altering the genetic code), protein levels and metabolic indicators across different tissues.
The findings showed consistent changes across many tissues that opposed typical ageing patterns. However, researchers emphasised several important limitations to their work.
The results were observed only in mice, not humans, meaning whether the drug has any real effect on human ageing remains unknown. The study was conducted on middle-aged mice, so the effects might not be the same in very old animals.
Additionally, while the drug appeared to induce many molecular signs of younger age across tissues, the study did not prove that actual biological ageing was reversed or that the mice lived longer.
GLP-1 receptor agonists work by binding to receptors that respond to the GLP-1 hormone. This binding triggers metabolic processes, including insulin release and appetite suppression, and potentially, as this study suggests, molecular changes linked to younger biological age.
The researchers hope their findings will lead to larger clinical trials and help in developing anti-ageing drugs. However, they stress that longitudinal studies tracking subjects over extended periods are necessary to determine whether these drugs could form part of a comprehensive anti-ageing strategy.
The growing interest in using diabetes and weight-loss drugs for longevity reflects wider trends in anti-ageing research, where scientists increasingly examine how existing medicines might have benefits for healthspan and lifespan.
Experts caution that people should not start taking these medicines for anti-ageing purposes based on animal studies alone, as human trials are needed to establish safety and efficacy for this use.
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