Failing Mitochondrial Quality Control in Aging and Neurodegeneration

Every one of our cells contains hundreds of mitochondria, the descendants of ancient symbiotic bacteria now fully integrated into our biochemistry. Mitochondria contain their own small remnant genome, the mitochondrial DNA, replicate like bacteria, and toil to produce adenosine triphosphate (ATP), a chemical energy store molecule used to power cell processes. Mitochondrial function declines with age, unfortunately, and our cells suffer for it. This contributes meaningfully to many age-related conditions. This decline appears to result in large part from changes in gene expression that impair the various quality control processes that (a) ensure mitochondrial proteins are correctly formed, and (b) that damaged mitochondria are recycled. Those changes in gene expression are maladaptive responses to other aspects of aging, perhaps in part the shift to an inflammatory environment, perhaps in part due to changes in nuclear structure resulting from cycles of double strand DNA repair, and so forth. The search for ways to improve mitochondrial function in old age is an area of considerable focus in the aging research community and longevity industry. Partial reprogramming is perhaps the most well funded approach, but numerous efforts are being undertaken to find ways to improve mitochondrial quality control to greater degrees than can be achieved via supplements and exercise. Beyond this, a number of groups are building the infrastructure needed to manufacture large amounts of...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs