Calcium channel linked to familial advanced sleep phase and how it shifts our internal clock
Official title: Characterizing a Calcium Channel Causing FASP: Examining Entrainment Changes as a Mechanism for Phase Advance
Funded at University of California, San Francisco · NIH-11604341 · Data updated 2026-11-12
This project studies a genetic change in a calcium channel that may cause very early sleep times and waking times in families, with potential to guide future treatments for advanced sleep phase.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of California, San Francisco NIH-funded |
| Lab location | 1 site (San Francisco, United States) |
| Project start | September 18, 2026 |
| Project end | August 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $574,000 |
| NIH project number | 1R56NS144190-01 |
| Project ID | NIH-11604341 on NIH RePORTER |
Who could benefit from this research
✓Could help
Individuals with familial advanced sleep phase or related circadian rhythm disorders may be eligible for future translational studies or trials.
✕Less likely to help
People without a circadian rhythm disorder similar to FASP are less likely to benefit from this specific genetic focus.
What this research studies
Researchers have identified a genetic variant in CACNA1D linked to familial advanced sleep phase, causing very early bedtimes and wake times in children and young adults. The project includes sequencing of affected families, functional tests in cells, and a mouse model to understand how these variants alter circadian timing. The goal is to uncover how a specific calcium channel change can advance the body's internal clock and whether this could lead to new ways to manage sleep timing problems. This work could pave the way for targeted therapies that help people align sleep schedules with daily demands.
Why it matters
Potential benefit: If successful, the findings could inform new approaches to treating very early sleep schedules and improve quality of life for people with FASP.
How similar studies have gone: Previous work has linked CACNA1D variants to circadian phenotypes and mouse models provide supporting evidence, but human gene-phenotype links remain an active area.
Where this research is happening
-
University of California, San Francisco
San Francisco, United States Active
Researchers
- Principal investigator: Ptacek, Louis J. — University of California, San Francisco
- Study coordinator: Ptacek, Louis J.
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.