Campaign run · Alzheimer's disease
ideate-alzheimer-mechanism-r2
Research purpose: understand the MECHANISM of Alzheimer's disease (AD) — the molecular, cellular, circuit, and systems-level processes that drive selective neuronal vulnerability and disease progression (amyloid-β, tau/NFTs, APOE & genetics/GWAS, microglia & neuroinflammation, synaptic loss, vascular/BBB dysfunction, lysosomal-autophagy, astrocytes) — and propose PROMISING FUTURE RESEARCH DIRECTIONS that are concrete enough for an autonomous computational pipeline to pursue on PUBLIC data.
Status
- How far it got
- Ideation only
Ended after surveying the field and proposing research directions, by design. Ideation-only runs do not nominate hypotheses.
- Why it stopped
This was an ideation-only run. By design it surveyed the field and proposed research directions, then ended. It was never meant to pre-register or test hypotheses, so it has none.
- Recorded status
Halted. The run recorded a final status of halted: it was closed without being marked done. A halted run can still have tested hypotheses and written a final report.
- Census class
Early stop. Census class is a label from an earlier, process-level census of the campaign. It does not map one-to-one onto the stages above. How the classes compare.
Research question
The sentence under the run id is quoted from this brief.
Full research brief given to the run
Research purpose: understand the MECHANISM of Alzheimer's disease (AD) — the molecular, cellular, circuit, and systems-level processes that drive selective neuronal vulnerability and disease progression (amyloid-β, tau/NFTs, APOE & genetics/GWAS, microglia & neuroinflammation, synaptic loss, vascular/BBB dysfunction, lysosomal-autophagy, astrocytes) — and propose PROMISING FUTURE RESEARCH DIRECTIONS that are concrete enough for an autonomous computational pipeline to pursue on PUBLIC data.
Targets:
(1) Survey AD-mechanism evidence broadly: papers (single-cell/spatial atlases, genetics/GWAS, proteomics, amyloid-β biology, tau/NFT pathology, microglia/neuroinflammation, synaptic loss, vascular/BBB, lysosomal-autophagy, astrocytes, selective neuronal vulnerability e.g. entorhinal cortex / EC), plus stated positions from leading AD researchers and relevant philosophy-of-medicine views on causation/biomarkers (e.g. the amyloid-cascade debate).
(2) Propose directions that are NOVEL relative to the campaign's existing topics — do not re-propose work already covered; find the gaps and the cross-cutting syntheses between them.
(3) For each proposed direction, identify CANDIDATE PUBLIC DATASETS (named atlases / accessions / repositories: GEO, SRA, PRIDE, Synapse, cellxgene, EBI, Allen, ADNI-derived public tables, etc.) that the direction would use. Put dataset pointers in the direction's rationale.
IMPORTANT — downloadability: prefer OPENLY-DOWNLOADABLE datasets (GEO supplementary, Synapse-open, cellxgene, EBI) so that the downstream EXECUTE stage can actually fetch the data. For any dataset that is access-controlled (dbGaP, controlled ROSMAP, controlled SEA-AD), EXPLICITLY FLAG it as access-controlled, since fetching it requires an application. As examples it may consider, well-known OPEN human AD single-cell/transcriptomic datasets (treat as candidates and VERIFY accessions — do not assume): Mathys 2019 (prefrontal cortex snRNA-seq), Grubman 2019 (candidate GSE138852, entorhinal cortex), Lau 2020 (candidate GSE157827, prefrontal cortex), Leng 2021 (entorhinal + superior frontal gyrus), Morabito 2021 (candidate GSE174367, snRNA + snATAC), Gerrits 2021, Sayed 2021.
This is a survey + proposal task, not a data-analysis task.
The research question comes from the topic's current research brief. All attempts at a topic share it; earlier attempts may have started from an earlier wording.