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Every row of the evidence table
One row per finding: what was tested, which way the result went, and how the study was built. The answer by area, and where the studies disagree, are on the main page.
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Showing 2 of 382 rows for TREM2 variants. One row per study per exposure: a study that tested two different things appears twice, once for each.
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| Exposure | Question | Direction | Outcome measured | Design | People | Effect size, as the source reported it | Source |
|---|---|---|---|---|---|---|---|
| TREM2 variants Genes (not modifiable) | Prevention |
Harm
whyDirection is for carrying TREM2 T96K: it increased AD risk in family-based and case-control sequencing data and, despite being a gain-of-function variant, impaired microglial clustering around plaques, amyloid uptake and the transition to disease-associated microglia in female 5xFAD mice. |
AD risk in a whole-genome sequencing dataset, and microglial plaque clustering, amyloid uptake and disease-associated transition in female 5xFAD knock-in mice | None | not stated | not established — pubmed abstract reports no numeric effect size (no odds ratio for the risk association is printed). |
Neuron
2026 ✓ Peer-reviewed PMID 41109213 |
| TREM2 variants Genes (not modifiable) | Prevention |
Harm
whyDirection is for carrying the risk variants: R62H and T96K caused excessive skipping of exon 2 and overproduction of a potentially antagonistic TREM2 isoform, and several early-onset dementia variants acted primarily through splicing defects. A molecular mechanism result, not a clinical outcome. |
TREM2 exon 2 skipping and isoform production in variant carriers | None | not stated | not established — pubmed abstract reports no numeric effect size. the library had recorded "1.8-fold increase in exon 2 skipping in r62h carriers", which the abstract… |
Brain
2024 ✓ Peer-reviewed PMID 38226698 |