Since mitochondria seem to be the dominant theme this week, today I thought I’d point out a couple of recent open access papers that focus on the role of mitochondrial function (and dysfunction) in the neurodegeneration that accompanies aging. Every cell bears a swarm of mitochondria, the descendants of ancient symbiotic bacteria. Even though mitochondria long ago evolved into integrated cellular components, they still behave very much like bacteria in many ways. They multiply through division, and can fuse together and swap component parts, pieces of the molecular machinery necessary to their function. They also contain their own DNA, distinct from that of the cell nucleus.
The primary role of mitochondria is to undertake the energetic process of packaging chemical energy store molecules to power cellular operations. This is of particularly importance to energy-hungry tissues such as the brain, and why mitochondrial dysfunction with advancing age is thought to be especially relevant to neurodegenerative conditions. The evidence for this is more clear or less clear depending on which condition is discussed. In Parkinson’s disease, for example, it is very evident that mitochondrial function is central to the characteristic loss of specialized neurons that drives the condition.
Article originally posted at