# Longevity Nerd

- **Event:** [Built with Claude: Life Sciences](https://cerebralvalley.ai/e/built-with-claude-life-sciences)
- **When:** Jul 7 at 12:00 PM – Jul 14 at 12:00 AM (EDT)
- **Where:** Online
- **Team:** [Naisha Shah](https://cerebralvalley.ai/u/longevity_nerd)
- **GitHub:** https://github.com/naisha-shah/ClaudeScience_Hackathon
- **Demo video:** https://youtu.be/eOJRm_Jpr9g
- **Gallery:** https://cerebralvalley.ai/e/built-with-claude-life-sciences/hackathon/gallery
- **Page:** https://cerebralvalley.ai/e/built-with-claude-life-sciences/hackathon/gallery/229

APOE genotype is fixed at birth, yet Alzheimer's appears decades later. We asked whether the fixed APOE ε2/ε4 plasma-protein substrate (Lu 2026) interacts with the age-emergent proteome — three proteomic waves (Lehallier 2019) and many organ and cell-type aging clocks (Ding 2026, Oh 2023) — by testing protein-network coupling across five interactomes and two states (plasma and brain), against degree-matched nulls.
Network-wise, the two programs are largely segregated across most aging and aging-related changes and both alleles — especially ε2. One moderate overlap sits at ε4 × later-life aging (the ~78-year wave), carried by a lipoprotein/ECM arm (APOM, FBLN1 → CLU, APOL1, FN1), an inflammatory arm (IL6ST, KITLG, RGMA → IL6 / STAT3, KIT) and a neuronal arm (NEGR1, NPTX2, NRXN1, GFRA2). Independent human genetics give these proteins support for causality inference — CLU in Alzheimer's, FN1 in coronary artery disease — and both are potential drug targets, with CLU-raising compounds already showing preclinical Alzheimer's efficacy (Cohn 2025).
Built and stress-tested two ways with Claude Science: one chat end-to-end, and a multi-chats system passing results through shared artifacts.

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Markdown version of https://cerebralvalley.ai/e/built-with-claude-life-sciences/hackathon/gallery/229. Site index for agents: https://cerebralvalley.ai/llms.txt · full text: https://cerebralvalley.ai/llms-full.txt