Max A. Thorwald

ApoE isoforms establish distinct antioxidant trajectories across the aging brain

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.

Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age

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.

Induction of ferroptotic and amyloidogenic signatures linked to Alzheimers disease by chemically distinct air pollutants

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

Form and function of actin impacts actin health and aging.

This study investigates how actin structure and function affect aging in C. elegans and finds that actin dysfunction accelerates aging hallmarks and correlates with human age-related decline in gait speed.

17α-Estradiol Confers Limited Protection Against APOE4 Phenotypes in Middle-Aged Female Mice

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

The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome

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.

Single cell profiling reveals GSM-15606 attenuates air pollution-induced inflammation and preserves hippocampal neurogenesis

The paper uses single-cell RNA sequencing to show GSM-15606 reduces inflammation and preserves neurogenesis in the hippocampus of mice exposed to air pollution.

Chimpanzee and human ApoE isoforms differ in the stimulation of neurite differentiation consistent with structural predictions with relevance to brain development and aging

The paper shows chimpanzee ApoE isoforms increase neurite number but reduce neurite length compared to human ApoE isoforms, suggesting functional similarity to ApoE4.

Down syndrome with Alzheimers disease brains have increased iron and associated lipid peroxidation consistent with ferroptosis

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.

Iron chelation by oral deferoxamine treatment decreased brain iron and iron signaling proteins

The paper shows oral DFO reduces brain iron and iron-related proteins in mice, suggesting potential therapeutic benefits for early-stage Alzheimer's.

Iron associated lipid peroxidation in Alzheimers disease is increased in lipid rafts with decreased ferroptosis suppressors, tested by chelation in mice

The paper investigates iron-mediated toxicity in Alzheimer's disease by analyzing postmortem brain tissue and ApoE4 mice, finding increased lipid peroxidation and decreased antioxidants in lipid rafts, which are reduced by iron chelation.

Activation of the muscle-to-brain axis ameliorates neurocognitive deficits in an Alzheimer disease mouse model via enhancing neurotrophic and synaptic signaling

This study shows that enhancing the muscle-to-brain axis in Alzheimer's disease mice reduces amyloid plaques and improves cognitive function through neurotrophic and synaptic signaling.

Protection against APOE4-associated aging phenotypes with the longevity-promoting intervention 17α-estradiol in male mice

This study shows that 17α-estradiol improves aging outcomes in APOE4 mice more than APOE3 mice, suggesting a genotype-dependent benefit of the intervention.

Transcript errors generate a continuous stream of amyloid and prion-like proteins in human cells

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