The short version
I'm a PSEN1 carrier. If you know what that means, you already get why I read papers the way some people follow sports. If you don't: PSEN1 is one of the genes tied to early-onset familial Alzheimer's. Getting that result rearranges how you think about time — and about the biology underneath it.
I could've treated it as a countdown. I decided to treat it as a research question instead. And that question kept dragging me toward the mitochondria — the tiny power plants in every one of your cells — and then, very specifically, to one little doorway on their surface: VDAC1.
Why mitochondria, why VDAC1? Mitochondria don't just make energy — they hold the switches for inflammation and cell death too. And VDAC1 sits right at the crossroads: metabolites pass through it, calcium passes through it, and when a cell is in trouble it's part of how the mitochondria decide to pull the plug. For a disease where hungry neurons slowly fail, that crossroads looks awfully important.
My journey into mitochondrial research
I didn't show up with a PhD and a lab. I showed up with a genetic result, a stubborn streak, and PubMed. I started reading to understand my own risk, and I kept reading because the story got better the deeper I went.
What hooked me was noticing how often the amyloid-centric story of Alzheimer's leaves the energy problem in the footnotes. Neurons are absurdly power-hungry. Mitochondria are how they eat. When mitochondrial quality control slips — when damaged mitochondria leak, when VDAC1 starts oligomerizing and opening pores, when mtDNA ends up where it shouldn't and the immune system panics — you get exactly the slow-burn inflammation and cell loss that neurodegeneration is made of.
So I made it a project: read the primary literature, follow the interesting labs, track the drugs, and keep a plain-language map of the whole thing. This blog is that map, out in the open.
The co-founder hat
Alongside the reading, I'm a co-founder at x-tosis — a Gainesville, Florida biotech developing first-in-class VDAC1-modulating mitochondrial therapeutics for neurodegeneration (Alzheimer's, Parkinson's, ALS). Yes: the exact mechanism this whole blog circles is also my day job. That's not a coincidence — the reading and the building grew out of the same obsession. Working on the company side keeps me honest, too: it's one thing to find a mechanism beautiful in a paper, another to think about what it'd actually take to move it toward people.
To be clear about the wall between the two: this blog is my personal notebook, not a company channel. When x-tosis comes up here, I flag it. Opinions are mine, they're not investment advice, and they are definitely not medical advice.
What you'll find here
Three things, mostly: news — recent papers summarized in plain words and linked to the source; resources — the reviews, databases and labs I keep coming back to; and explainers — my attempts to make this stuff make sense to a smart non-specialist, because that's exactly who I was when I started.
I write casually on purpose. It's a passion project, not a journal submission. If I get something wrong — and I will — please tell me. Half the fun is being corrected by people who know more.
Say hi. I genuinely like hearing from people — researchers, fellow carriers, patients, the merely curious. shinaoffer@gmail.com.