Every day, I bookmark several recent papers, hoping to get back to them shortly with a close reading and a review. I’m realizing that the rate of appearance of worthwhile material far outstrips my ability to keep up, and I have to skip some interesting articles. Instead of consigning these to Davy Jones’ locker, I will instead compile them weekly in one-liner format, so that You The Reader have the chance to check out intriguing stories on your own.

Here goes:

DNA damage: Age-dependent accumulation of recombinant cells in the mouse pancreas revealed by in situ fluorescence imaging, Wiktor-Brown et al.

This work demonstrates that aging and exposure to a cancer chemotherapeutic agent increase the frequency of recombinant cells in the pancreas, and it also provides a rapid method for revealing additional factors that modulate HR and clonal expansion in vivo.

DNA repair: Haploinsufficiency in DNA Polymerase ß Increases Cancer Risk with Age and Alters Mortality Rate, Cabelof et al.:

…the ß-pol+/– mouse represents a model in which mortality rate and tumor development are accelerated and provides evidence supporting the role of genomic maintenance in both aging and carcinogenesis.

Mitochondria and hearing loss: Role of mitochondrial dysfunction and mitochondrial DNA mutations in age-related hearing loss, Yamasoba et al.

Together these findings indicate that decreased energy metabolism due to accumulation of mtDNA mutations/deletions and decline of respiratory chain function play an important role in the manifestation of AHL.

Calorie restriction: Influences of calorie restriction and age on energy expenditure in the rhesus monkeys, Raman et al.

Caloric restriction (CR) is known to retard the aging process and a marker of aging is decreased energy expenditure (EE). … In conclusion, CR did not alter the age-related decrease in EE with CR.

Glycation and diet: Glycotoxins and cellular dysfunction. A new mechanism for understanding the preventive effects of lifestyle modifications, Michalsen et al. (German)

Advanced glycation end products (AGEs) are the derivatives of glucose-protein or glucose-lipid reactions and are mainly generated from the diet (depending on intensity of heating, cooking time and oxygenation). … The clinical impact of low-AGE diets and fasting and the interaction between stress and food intake should be further investigated in controlled trials.

Gene regulation and lifespan: Extraordinary plasticity in aging in Strongyloides ratti implies a gene-regulatory mechanism of lifespan evolution, Gardner et al.

Thus, the 80-fold difference in their lifespans, the greatest plasticity in aging yet reported, must largely reflect evolved differences in gene expression. This suggests that interspecific differences in lifespan may evolve via similar mechanisms.

Immunology and inflammation: The immune risk phenotype is associated with IL-6 in the terminal decline stage: Findings from the Swedish NONA immune longitudinal study of very late life functioning, Wikby et al.

In the present NONA immune longitudinal study, we further examine the previously identified T cell immune risk phenotype (IRP), relative inflammatory activity, morbidity and 2-year mortality in very old individuals >90 years. … Intriguingly, we also found that rare individuals moved out of the IRP category by a process of immune suppression, including increases in IL-6 and IL-10 and decreases in the number of CD3+CD8+CD28− cells.

(This seems like a good place to point out that the more other researchers volunteer to join this project, the more papers we’ll be able to treat in depth. If you are biologist of aging, a good writer, and find yourself obsessively reading Pubmed during electrophoreses, you might want to consider getting in touch.)