Marc Vermulst

This study shows ApoE isoforms influence antioxidant pathways differently across aging, with ApoE4 showing stronger transcriptional responses but less effective protein production, linking to neurodegenerative risk.

This study shows that mtDNA mutations arising early in life drive age-related pathologies and that mitochondrial fusion modulates their selection, suggesting interventions targeting fusion could slow aging.

This study shows that metal-rich air pollutants induce ferroptosis and amyloidogenic pathways linked to Alzheimer's disease through shared transcriptional and oxidative mechanisms.

This study tests if 17α-estradiol benefits APOE4 females similarly to males, finding limited CNS improvements but some metabolic benefits in APOE4 females.

This study shows that reduced IGF-1 signaling extends lifespan in mammals but not in mitochondrial mutator mice, indicating that mitochondrial genome stability is essential for the longevity benefits of IGF-1 suppression.

The paper examines iron levels and lipid peroxidation in DSAD brains, finding increased iron and lipid damage compared to AD and controls, suggesting ferroptosis involvement.

MADDD-seq detects DNA damage and mutations simultaneously in yeast using a modified double barcoding sequencing approach, revealing repair kinetics and mutagenesis over 24 hours.

The paper shows transcript errors generate amyloid and prion-like proteins in human cells, linking DNA damage to aging and disease.

This study uses cryo-EM to show that tau filaments in ALS/PDC share the CTE fold, suggesting environmental causes for the disease.

The paper estimates transcription fidelity in human cells, identifies factors controlling its accuracy, and links transcription errors to Alzheimer's disease progression.

The paper identifies a genetic variant in C. elegans atg-5 that alters autophagy's effect on polyglutamine aggregation, showing tissue-dependent outcomes.