Familial advanced sleep phase syndrome (FASPS) is a syndrome that requires early bedtime and early rising and differs from the sleep-wake rhythm of the vast majority of the population. FASPS is closely related to the human Period 2 (hPER2) gene, a key gene for important biological clock resetting in response to light factors. In addition, researchers obtained a transgenic mouse model of the FASPS hPER2 S662G mutation and found that phosphorylation of the S662 position leads to increased PER2 transcription, as well as phosphorylation of the other locus causes degradation of Per2. Changing the dose of CKIδ can alter the S662 phenotype, suggesting that CKIδ can regulate the timing in vivo by regulating per2. These findings have important implications for understanding human circadian rhythm-regulating genes. Whether she wants to or not, Madbrook gets up “on time” every morning between 1:30 and 3 a.m. She says, “I’m wide awake by then, and I’m ready to start painting my house without even a cup of coffee, not at all. ” But by 4 to 5 p.m. every day, she becomes drowsy again, and her biological clock is completely different from most people’s. Medbrook, 49, is a resident of Vermont, U.S. She suffers from a condition known as familial advanced sleep phase syndrome (familial advanced sleep phase syndrome). She goes to bed between 5:30 p.m. and 7:30 p.m. every day and wakes up in the early morning hours of the second day, unlike the majority of people in the world who have a different sleep-wake rhythm. The end result of this syndrome, Medbrook says, “is that I feel very lonely because no one wants to party at 3 a.m.” So she had to spend the long hours alone by quietly tidying her room, preparing breakfast or simply cuddling up with a book. Researchers say only a small percentage of the world’s population suffers from this familial early sleep state syndrome, which includes Madbrook’s mother, two sisters and daughter. University of California, San Francisco (UCSF) neuroscientist Hui Fu and her team conducted in-depth research specifically on this sleep cycle disorder. They found that a new mutation in a single gene is responsible for familial early sleep state syndrome, but scientists are not yet sure how the mutation changes people’s sleep schedule. The lab results show that the mutation makes a protein called CKIδ less active. In the next step of the study, scientists want to figure out what’s going on, Fuhui said. Carl? Hunter is the head of the Sleep Disorders Research Center at the National Institutes of Health in Maryland. He said the study has brought attention to the important role played by genes that regulate sleep, and perhaps more importantly, the study can determine why certain people have distinctive sleep habits. Fuhui said more than 10 tightly intertwined genes control the body’s biological clock, which in turn controls certain changes in physical and behavioral cycles, including changes in heart rate, blood pressure and the immune system. All of these cycles have been collectively referred to as circadian rhythms, which generally take a 24-hour day and night cycle. Back in 2001, Hui Fu and her colleagues identified another genetic mutation that can cause familial early sleep state syndrome. But the researchers noted that this mutation was not a common phenomenon among all family members with the disorder. This forced the researchers to continue to look for another genetic factor that could cause the disorder. They found mutations in CKIδ in five members of a family with the disorder in three generations. In addition to familial early sleep state syndrome, four of these five individuals experienced depressed mood and depression. Depressed mood, or depression, is likely to be due to the same causes,” said Ying-Hui Fu. As we further investigate why genetic mutations cause such sleep problems, we are likely to learn what causes depressed mood.” Sleep disturbance is a very prominent problem among people with depression, and there may be an important link between the two.