Meeting with Dr. Erika Taylor today

Septemeber 5, 2025

1. Dr. Erika says she would like to have a first meeting with folks who have their genetics returned to teach them what to look for preliminarily (individually). That is part of her job at Sequencing. Then later we would propose a meeting post cohort genomic evaluation.

   
   

2. She has not yet met with the IRB (Institutional Review Board) folks, as the University just got back into the swing of things. (She was also away and then got sick).

   
   

3. She wrote to both Ryan and Ev from Sequencing, asking to make sure all of our kits are on track. She says she will explore what happened with the two kits that haven't arrived.

   
   

4. We discussed her taking a look at modifier genes and she said "of course". She explained that some genes are located on areas of chromosomes that might be problematic to see, but that she'd explain more if that is relevant.

   I'm going to get sciency for a moment...I had asked her if it is possible that we might not see a tight ion-channel “signature,” and that the "architecture" is instead modifier-heavy—with RAAS/kallikrein-kinin/NO and other vasomotor genes shaping the phenotype?

   (MEANING, can we look at the genes involving support of the vasculature systems involved in sleep). This wouldn’t undercut the SOVM framework; it would simply suggest that the issue may be network-level (oscillatory gating ↔ neurovascular tone ↔ autonomic coupling), which is highlighted in the Oscillatory Overview and relevant to Dr. Lanza's research.

   
   

5. As an aside, ChatGPT described this as being “architecture-agnostic” and that SOVM may reflect either (A) subtle channel burden affecting state-boundary oscillations, or (B) vasomotor modifier genes (RAAS/kinin/NO) destabilizing neurovascular coupling at sleep onset. In my own case, there is clear Renin-Aldosterone-Angiotensin conversion issue with associated genetic variants, in addition to subtle channel burden (so, A and B).

6. Here are potentinal candidate modifier genes of interest (vascular/RAAS/autonomic):

   RAAS: ACE, ACE2, AGT, REN, AGTR1, AGTR2

   Kallikrein–kinin system: KLKB1, KNG1, BDKRB1, BDKRB2

   Vascular/autonomic tone: NOS3 (eNOS), GUCY1A1, GUCY1B1, PDE5A, ECE1

   Peptidases impacting bradykinin/angiotensin turnover: MME (neprilysin), XPNPEP2, CPB1, CPB2, DPP3