One of the recent New York Academy of Sciences web features is a nice focus on mitochondria and neurodegeneration. As I'm sure you know, mitochondria are complex little cellular components responsible for turning food into a more convenient, standardized source of energy for cells; they also produce "chemical waste" in the form of damaging free radicals. Beyond that, there are any number of external influences that can change the way in which mitochondria behave. More effort in recent years has been going towards determining the mechanisms by which mitochondrial changes and damage are linked to age-related disease.

David Nicholls of the Buck Institute for Age Research in Novato, California, has studied mitochondria for 40 years. In his talk at the Academy, he began by discussing recent advances in techniques with which to study mitochondrial bioenergetics in intact neurons. His experimental setup allows one to measure oxygen respiration while also monitoring a variety of other dynamic cell processes, such as mitochondrial membrane potential, plasma membrane potential, cytoplasmic calcium concentration, and the presence of reactive oxygen species [ROS]. Nicholls described dynamic interactions between mitochondria and the rest of the cell, interactions that were previously unknown but are now being revealed with his techniques.

Nicholls found that in many instances of cell failure, ROS are a red herring - a symptom rather than a cause. One example that stands out is that of glutamate excitotoxicity, in part because it has been studied so much. When neurons are continuously exposed to glutamate, calcium rushes in. Cells can maintain a holding pattern for a short period of time, but then succumb. Nicholls showed that ROS were present, but they did not interrupt the holding pattern. Instead, changes in the respiratory capacity of mitochondria were linked with triggering neurons' demise.

As we know, mitochondrial-generated ROS contribute to cellular changes that lead to age-related degeneration; the link is most clear for atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease - but there are many other potential problems that can result. For specific conditions, it is not always the case that this background age-related trend towards more damaged mitochondria and more ROS is at the root of the problem, however.

More information is more information, and it will all be useful at some point. An increase in resources dedicated to the study of mitochondria - prompted by advances in understanding in other fields - can only help in the long term. The results build a foundation for increased capabilities and funding to develop ways to repair age-related mitochondrial damage.

Technorati tags: biotechnology

Posted by Reason at November 10, 2006 4:19 PM | TrackBack (0)