Matt R. Kaeberlein

The paper analyzes the canine gut microbiome across 900 dogs to identify factors influencing microbiome composition and develops a metagenomics-based aging clock.

This study screens FDA-approved compounds in yeast and C. elegans to identify potential Alzheimer's disease treatments, finding that fluphenazine reduces amyloid-beta accumulation.

This study identifies molecular factors and pathways associated with genotype-dependent lifespan variation in response to caloric restriction in wild yeast isolates.

This study investigates vortioxetine's anti-cancer effects on glioblastoma cells using cell viability and migration assays, showing suppression of cell growth and survival.

This study shows that reducing folate intake in aged mice decreases biosynthetic processes but does not compromise healthspan, suggesting age-dependent benefits of folate restriction.

The paper investigates how knocking out nuclear-encoded mitochondrial genes in yeast affects lifespan, revealing shared mechanisms involving ribosomal proteins, actin dynamics, and proteasome function.

This study uses multidimensional proteomics to analyze age-related changes in yeast cells, identifying molecular trajectories of aging and rejuvenation.

The paper shows that iron status affects disease progression in Complex I-deficient mice, with iron restriction delaying symptoms and increasing survival.

The paper shows that reducing Cth2 activity in yeast increases lifespan by improving mitochondrial function through reduced repression of iron-related genes.

The paper analyzes lifespan variation in wild yeast isolates to identify genetic and environmental factors shaping replicative lifespan and cellular processes involved in aging.

This study shows that the prion [BIG+] in yeast increases proliferation but reduces lifespan by altering protein synthesis and translational programs.

The paper identifies PKC as a therapeutic target for treating mitochondrial disease by analyzing proteomic and phosphoproteomic changes in a mouse model of Leigh syndrome.

The paper analyzes longevity interventions across species and identifies a structured 'landscape of longevity' with soft bounds on achievable lifespan, including a human upper limit of ~138 years.

The paper identifies translational control of methionine and serine metabolic pathways as the mechanism underlying paralog-specific phenotypes in Rpl22 ribosomal protein mutants, linking these changes to cell division and replicative longevity.

The paper shows that loss of vacuolar acidity in yeast causes iron sulfur cluster defects and divergent iron homeostasis during aging.

The paper identifies hsp-16.2 chaperone biomarkers as indicators of proteome dosage states in C. elegans, revealing cell-to-cell variation linked to gene expression differences.

This study edits rDNA replication origins in yeast using CRISPR/Cas9, revealing growth and lifespan consequences of such modifications.

The paper quantifies Intron Mediated Enhancement (IME) in C. elegans by measuring protein expression levels using fluorescent reporters and finds a single intron can increase expression by about 50%.

This study uses single-cell imaging to examine age-related genome missegregation in yeast, identifying rDNA expansion as a contributor to mitotic failures and nucleolar breakdown.

DECODER integrates large-scale gene expression data to identify mitochondrial Complex I as a therapeutic target for Alzheimer’s disease.