How brain calcium channels and CaMKII convert nerve activity into gene signals
Calcium Channels, CaMKII and Mechanisms of Excitation-Transcription Coupling
['FUNDING_R01'] · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · NIH-11377351
This work looks at how calcium channels and the protein CaMKII let brain cells turn electrical activity into gene signals that support memory and may matter for people with Alzheimer's disease.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | NEW YORK UNIVERSITY SCHOOL OF MEDICINE (nih funded) |
| Locations | 1 site (NEW YORK, UNITED STATES) |
| Trial ID | NIH-11377351 on ClinicalTrials.gov |
What this research studies
From a patient's perspective, scientists will trace how L-type calcium channels in neurons set off signals that reach the nucleus and switch on memory-related genes, focusing on the roles of CaMKII and the CREB protein. They will examine both calcium entry and a voltage-driven shape change (VΔC) of the channel to see how these signals cooperate with glutamate receptors to boost gene activation. Experiments use laboratory neurons and model systems to follow calcium, protein movement, and CREB phosphorylation, and to measure effects on synapses and molecular dynamics. The goal is to map the key steps that support learning and to identify where the process can fail in brain disorders like Alzheimer's.
Who could benefit from this research
Good fit: This research is most relevant to people with Alzheimer's disease or age-related memory loss and to those who might donate tissue or biological samples or join related future clinical studies.
Not a fit: People with medical conditions unrelated to brain function or memory are unlikely to see direct benefits from this basic lab-focused work in the near term.
Why it matters
Potential benefit: If successful, this could reveal molecular targets to protect or restore memory-related gene signaling and guide future therapies for Alzheimer's disease.
How similar studies have performed: Previous laboratory studies have linked L-type calcium channels, CaMKII, and CREB to synaptic plasticity and memory, but applying the detailed mechanisms to Alzheimer's-related dysfunction remains early-stage and partly novel.
Where this research is happening
NEW YORK, UNITED STATES
- NEW YORK UNIVERSITY SCHOOL OF MEDICINE — NEW YORK, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: TSIEN, RICHARD W — NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- Study coordinator: TSIEN, RICHARD W
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 below.
Conditions: Alzheimer disease dementia, Alzheimer syndrome, Alzheimer's Disease