ArticleCell biology and toxicology2026
ALKBH5-mediated m6A demethylation of PRMT6 inhibits neuronal apoptosis and ferroptosis in Alzheimer's disease via reducing transcription of ACSL4.
Article in Cell biology and toxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundProtein arginine methyltransferase 6 (PRMT6) is confirmed to regulate Alzheimer's disease (AD) process. Acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated ferroptosis is involved in regulating AD progression. However, whether PRMT6 regulates AD progression through ACSL4-mediated ferroptosis is unknown.
methodsAD mice were injected with adeno-associated virus to explore the role of PRMT6 and AlkB homologue 5 (ALKBH5) in vivo. Neuronal cells were treated with amyloid-β protein fragment 1-42 (Aβ1-42) to mimic AD cell models. The expression levels of PRMT6, ALKBH5, ACSL4, GPX4, and SLC7A11 were tested by qRT-PCR or western blot. Cell viability and apoptosis were detected by CCK8 assay and TUNEL staining. The levels of ROS, MDA, SOD and Fe
resultsPRMT6 expression was upregulated in AD mice. Silencing of PRMT6 repressed Aβ1-42-induced neuronal cell apoptosis and ferroptosis, as well as alleviated cognitive deficits in AD mice. ALKBH5 reduced PRMT6 expression by inhibiting its m6A modification. ALKBH5 overexpression suppressed Aβ1-42 induced apoptosis and ferroptosis in neuronal cells, and this effect was reversed by PRMT6 upregulation. Besides, PRMT6 promoted ACSL4 expression via increasing H3R2me2a on the ACSL4 promoter, and ACSL4 overexpression also abolished the inhibitory effect of PRMT6 knockdown on Aβ1-42-induced cell ferroptosis. Meanwhile, ALKBH5 inhibited neuronal cell ferroptosis to relieve cognitive deficits in AD mice via repressing the PRMT6/ACSL4 axis.
conclusionALKBH5 could inhibit neuronal cell ferroptosis to alleviate the progression of AD by decreasing PRMT6-mediated ACSL4 transcription through H3R2me2a.
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