Improving memory is an eternal topic of concern for us. As people age, they will experience a decline in memory, which is a natural physiological law. Meanwhile, the most common symptom of some diseases, such as Alzheimer's disease, is a decline in memory. Is there any way to enhance a person's memory? Recently, a paper published in the journal Scientific Progress stated that neuroscientists have designed a synthetic protein that can promote memory function in elderly individuals with cognitive decline. They genetically modified the LIMK1 protein and embedded a synthetic peptide "molecular switch" that can be activated by immunosuppressive drugs, significantly improving the memory of experimental animals. This discovery brings hope to patients with Alzheimer's disease and other neurodegenerative diseases, and has the potential to "completely change the field of neurology.". How is memory formed? How does the synthetic peptide "molecular switch" work? Regarding these issues, a reporter from Science and Technology Daily interviewed Christian Ripoli, the first author of the paper and associate professor of science at the Catholic University of Sacred Heart in Italy, as well as Claudio Grasi, the senior author of the paper and head of the Department of Neuroscience at the Catholic University of Sacred Heart in Italy, as well as a professor of physiology and psychology. "Memory is a complex process that involves changes in synapses connecting neurons in specific areas of the brain, such as the hippocampus. This phenomenon of synaptic change is called synaptic plasticity," said Gracie. Ripley introduced the process of memory formation to reporters in an interview: "Memory is usually understood as explicit memory, which includes information about location, people, and objects. Clinical evidence and preclinical studies in mammals have identified key brain regions involved in signal processing and memory formation, including the hippocampus and related areas of the medial temporal lobe." In the neural circuits of these brain regions, synapses transmit information through electrical signals. These transmissions lead to protein modification, activation or inactivation, as well as changes in protein expression, which in turn trigger long-term changes in synaptic connectivity strength. The changes in these proteins can make people recall the activation of the same neurons at certain times, thereby helping to preserve and restore memory over time. So, how is memory enhanced and weakened? Lipli stated that this is related to LTP. Long term synaptic plasticity refers to the response of neuronal synapses to prolonged stimuli. LTP is an important long-term synaptic plasticity, which refers to the long-term enhancement of synaptic efficacy between neurons under certain stimulus conditions. Dendritic spines are the main site for the formation of synapses between neurons. And LTP occurs on dendritic spines. On dendritic spines, hundreds of proteins can alter their function during the occurrence of LTP. Dendritic spines enhance information transmission in neural networks and are crucial for learning and memory processes. Memory is regulated through this plasticity. LIMK1 is closely related to memory, according to Ripley. Unless influenced by LTP, dendritic spines maintain a relatively stable structure. The maintenance of structure depends on the opposite activity of two proteins (filamentin and actin). Actin naturally tends to aggregate,