The latest Rejuvenation Research is out, following closely on the heels of volume 9, number 1. I pointed out some of the items I found most interesting in that previous issue last month; this new issue is a sizeable one. My picks below hardly scratch the surface, and you'll find a lot to read.
Aging should be considered a major risk factor for life-threatening degenerative pathologies including atherosclerosis, cancer, neurodegeneration, diabetes type II, osteoporosis, and sarcopenia. ... Currently predominant disease-oriented paradigm should be reconsidered toward aging/longevity oriented.
This is a very important topic at the infrastructure and cultural levels of medical research; the present "discover and patch" methodology is inefficient - and ultimately ineffective - in comparison to a focus on repairing and preventing the root causes of aging.
The human mitochondrion contains a small circular genome that codes for 13 proteins, 22 tRNAs, and 2 rRNAs. The proteins are all inner membrane bound components of complexes involved in the electron transport system and ATP formation. Mutations to any of the 13 proteins affect cellular behavior because energy production could be decreased. Investigators have attempted to find methods to correct these mutated proteins. One way is to express the mitochondrial gene in the nucleus (called allotopic expression). The newly synthesized protein would have to be imported into mitochondria and assembled into complexes. This paper reviews some of the successful attempts to achieve allotopic expression and discusses some issues that might affect the ability to have the proteins properly inserted into the inner membrane.
More researchers are looking into ways to alleviate or prevent age-related damage to mitochondrial DNA - this is one area of basic anti-aging science in which funding from traditional disease-focused sources is plausible, given the strong (and growing) weight of evidence associating mitochondrial dysfunction with widespread and well-known age-related conditions.
Other groups are making progress in methods of replacing damaging mitochondrial DNA (mtDNA), a different approach to the SENS proposal of moving these genes into the comparatively well-protected nucleus. Competition and variety are good signs - may the best methodologies win.
Following on from this, a couple of papers demonstrate the positive effects of calorie restriction (CR) on mitochondrial function; not too surprising considering the relationship between the metabolic processes and damage to mitochondria. This sort of result lends strength to any claim that CR "slows aging" by showing a portion of how it does so - in this case by reducing the rate of one class of changes at the root of degenerative aging.
A decrease of the mtDNA content occurs with aging in liver and soleus muscle, whereas there is no age-related significant change of mtDNA content in brain. CR fully reverses the age-dependent loss of mtDNA in liver and soleus, whereas it results in a significant increase of mtDNA amount above the value of aged ad libitum fed rats in brain.
The present results show that CR largely prevents the age-associated decline in mitochondrial function in heart and skeletal muscles, and suggest that this is secondary to a better-maintained drive on mitochondrial biogenesis.