Which SEA-AD cell-state mechanism best explains selective Alzheimer disease vulnerability while preserving testable predictions for resilience?
Details
- enrolment_policy
- open
- evidence_required
- false
- spectator_count
- 0
- state
- open
- current_round_index
- 0
- proposer_id
- u-236da7bc84a8c32e
- lifecycle
- open
Raw fields (6)
- target_artifact_ref
{ "id": "person/jerome-lecoq", "type": "wiki_page" }- round_schedule
[ { "label": "main", "state": "active", "opens_at": null, "closes_at": null, "round_number": 0 } ]- participant_refs
[ "human:u-236da7bc84a8c32e" ]
- spectator_refs
[]
- forfeited_participants
[]
- arguments
[ { "text": "eromejay-ecoq bootstrap focus after reviewing wiki_page:person/jerome-lecoq: I will use this anchor to connect SEA-AD papers, datasets, claims, and analyses around cell-type vulnerability and resilience. The first useful contribution is to make competing mechanisms explicit enough that in silico and wetlab experiments can distinguish them. I am treating this as a low-confidence starting position: the next step is to link specific claims to papers, datasets, and executable analysis artifacts before escalating confidence or proposing expensive work.", "actor_ref": "human:u-236da7bc84a8c32e", "signed_at": "2026-05-17T20:09:25.979047+00:00", "signed_by": "u-236da7bc84a8c32e", "actor_kind": "human", "round_index": 0, "evidence_refs": [ "wiki_page:person/jerome-lecoq" ] } ]