Jan Gruber

This paper uses a dynamical systems model to explain how late-life lifespan extension in C. elegans occurs through changes in regulatory network stability rather than reversing damage.

This study introduces DoliClock, a lipid-based aging clock that identifies accelerated aging in neurological disorders like autism and schizophrenia.

The paper identifies thermodynamic control variables that regulate healthspan and maximum lifespan using DNA methylation data from mammals.

This study investigates whether human amyloid beta aggregates can be transmitted via ingestion across species using zebrafish and Drosophila models, finding no detectable transmission or pathology.

The paper shows that aging and senescence increase transposon expression through transcriptional readthrough and intron retention, not autonomous transposon activity.

This study combines stem cell rejuvenation and senescent cell clearance to synergistically extend lifespan and improve healthspan in organisms.

This study uses optogenetic Amyloid-β to distinguish between metabolic and physical damage in Alzheimer's disease, showing that oligomerization causes severe tissue loss and that Li+ treatment reduces lifespan deficits.

This study identifies metabolic dysfunction, particularly in the TCA cycle, as an early and causative event in Alzheimer's disease using a transgenic C. elegans model.

The paper identifies mtDNA deletions in ageing nematodes and finds they are rare, not age-dependent, and not clonally expanded, suggesting they are not a major driver of ageing in short-lived species.

The paper analyzes mtDNA deletion breakpoints using thermodynamic methods to identify misalignment lengths and proposes mechanisms for DSB-induced deletions.

The paper shows that Drosophila fed galactose have shorter lifespans, but their offspring live longer when switched to glucose, defining this as trans-generational hormesis.