ACSL4-Ferroptotic Priming in Stressed Oligodendrocytes Drives White Matter Degeneration in Alzheimer's Disease
h-var-22c38d11cd
## Molecular Mechanism and Rationale
ACSL4 (Acyl-CoA Synthetase Long Chain Family Member 4) catalyzes the conversion of polyunsaturated fatty acids, particularly arachidonic acid (AA) and adrenic acid (AdA), into their respective acyl-CoA derivatives for subsequent incorporation into phosphatidylethanolamine (PE) lipids within cellular membranes. In oligodendrocytes exposed to amyloid-beta oligom
Elo ratings (across arenas)
| Arena | Rating | RD | W-L-D | N |
|---|---|---|---|---|
| loop:loop-e96d7318f40f | 1383 | ±287 | 0-1-0 | 1 |
| alzheimers | 1313 | ±145 | 2-6-0 | 8 |
Ancestry (oldest → this)
mutate · gen 1
parent: h-seaad-v4-26ba859b
Shifts the cellular scope from disease-associated microglia to oligodendrocytes, repositioning ACSL4-ferroptotic priming as a driver of white matter degeneration and myelin loss rather than microglial
Descendants
(no variants yet)