Research roundup

Continuing the tradition I began last week, I give you some of the articles I would have treated at greater length last week if there were more of me (that is to say, more of us).

In no particular order:

Mitochondrial mutation: Mitochondrial DNA-Deletion Mutations Accumulate Intracellularly to Detrimental Levels in Aged Human Skeletal Muscle Fibers, Bua et al.,:

Deletion mutations were clonal within a fiber and concomitant to the COX-/SDH++ region. Quantitative PCR analysis of wild-type and deletion-containing mtDNA genomes within ETS-abnormal regions of single fibers demonstrated that these deletion mutations accumulate to detrimental levels (>90% of the total mtDNA).

Systems biology: Systems approaches to the networks of aging, Kriete et al.:

To increase our understanding of how aging works, we have to analyze and integrate quantitative evidence from multiple levels of biological organization. Here, we define a broader conceptual framework for a quantitative, computational systems biology approach to aging.

Melatonin: Melatonin treatment reverts aged-related changes in guinea pig gallbladder neuromuscular transmission and contractility, Gomez-Pinilla et al.:

Melatonin treatment for four weeks restored neurogenic responses to normal values, with an associated recovery of nitrergic function and the disappearance of the capsaicin-sensitive component. Aging also reduced the contractile responses to cholecystokinin (CCK) and Ca2+ influx.

Our favorite roundworm: Identifying factors that promote functional aging in Caenorhabditis elegans, Catherine Wolkow:

In C. elegans, aging leads to significant functional declines that correlate with muscle deterioration, similar to those documented for longer-lived vertebrates. This article will examine the current research into aging-related functional declines in this species, focusing on recent studies of locomotory and feeding decline during aging in the nematode, C. elegans.

Protein oxidation in Parkinson’s: Mutational analysis of DJ-1 in Drosophila implicates functional inactivation by oxidative damage and aging Meulener et al.:

Inherited mutations in PARK7, the gene encoding DJ-1, are associated with loss of protein function and early-onset parkinsonism. … Overoxidation of DJ-1 with age and exposure to oxidative toxins may lead to inactivation of DJ-1 function, suggesting a role in susceptibility to sporadic Parkinson’s disease.

Calorie restriction and mitochondria: Calorie Restriction in Mice: Effects on Body Composition, Daily Activity, Metabolic Rate, Mitochondrial Reactive Oxygen Species Production, and Membrane Fatty Acid Composition, Faulks et al.:

There was no CR-effect on in vitro reactive oxygen species production by liver or muscle mitochondria at 3 months, but after 6 months the effect was significantly reduced in liver mitochondria from 40 kcal/wk mice compared to 125 kcal/wk mice.