Reading the methods, it's clear the authors made *many* choices that likely affected the result. Here's a passage on the selection of technical covariates that caught my eye:

The authors compared gene expression between post-mortem and *living* brain tissue and found 80% (!) of genes were differentially expressed.

If true, this is a really big deal for any study using post-mortem brain tissue (i.e., nearly every study of human brain disease)

Come check out poster #745 at #AAIC and learn about how a healthy lifestyle can mitigate genetic predisposition to Alzheimer’s Disease!

We show that while these choices have increased the statistical power of recent AD GWAS, they have also potentially distorted the effect size of AD genetic associations. Here you can see effect size modification from different age cut-offs in the controls for example:

🎉📄Excited to share a pre-print of my most recent PhD project: "Downward bias in the association between APOE and Alzheimer’s Disease using prevalent
and by-proxy disease sampling in the All of Us Research Program" (short summary and link in replies ⬇️)

Really excellent keynote speaker @bionexuskc.bsky.social by Dr. Tatonetti and well said - “observation is the starting point of biological discovery.”

I typed “Super Bowl Watch Party” 🤦‍♂️

One of the coolest things we found was that the magnitude of the difference in CDR at visit 3 between the substance use history and cardiovascular history (0.45) was the same as reported in the Lecanemab trial!

Excited to share a preprint of my first project from my PhD: Distinct Medical and Substance Use Histories Associate with Cognitive Decline in Alzheimer's Disease! 🧠

doi.org/10.1101/2024...