aging tagged posts

With disease, when you decrease autophagy (a garbage disposal-like process where cells “eat” debris they produce) the disease process is exacerbated and when you increase it you get the opposite effect. Aggregation of polyglutamine expansion protein is a hallmark of Huntington’s disease and other neurodegenerative diseases. The picture shows that there are more aggregates of green fluorescence protein-labelled polyglutamine expansion protein in autophagy deficient worms (bottom) compared to normal worms (top).

In a human cell, CHIP (red) is recruited to clusters of a dementia-inducing protein (yellow). There is not enough CHIP for insulin receptor degradation in this situation. The cell undergoes premature aging. (Photo: CECAD)

ITGB3 (integrin β3) is regulated by the Polycomb protein CBX7 •β3 regulates senescence by activating TGF-β in a paracrine and autocrine fashion •β3 is highly expressed in OIS and induces senescence via ligand-independent pathway •There is a positive correlation between β3 levels and aging in different tissues

(a–c) Dose response effects on the median lifespan of select C. briggsae strains after treatment with chemicals that exhibited strong positive effects on the C. elegans strains. Dosing was performed only on strains that failed to respond positively in the initial tests (single dose experiments), as we did not attempt to identify peak responses, instead we only sought to identify whether positive effects could be obtained by altering doses. Chemical doses were chosen to center around the effective dose identified for C. elegans strains and were sometimes expanded after preliminary rounds of testing. ThT exhibited a positive effect on strain JU1348 at 25 μM, but was profoundly toxic to all strains at and above 100 μM