In this interview, a researcher focused on mitochondrial biochemistry discusses the role of these important cellular structures in aging and neurodegeneration, particularly Parkinson’s disease. There are really two ways of looking at mitochondria in aging. The first, the view incorporated into the SENS program, looks at damage to mitochondrial DNA and its consequences. A small but significant number of cells fall into a dysfunctional state because some forms of randomly occurring mitochondrial DNA damage can replicate rapidly within the cell, leading to cells that pollute their surroundings with reactive, harmful molecules. This might be addressed by providing backup copies of mitochondrial genes, a methodology known as allotopic expression.
The second view looks at mitochondrial dynamics and morphology, both of which change considerably in response to differences in the environment between old cells and young cells, old tissues and young tissues. This is a much more complex problem to consider, as no-one has yet mapped the chains of cause and effect that stretch from the fundamental forms of damage at the root of aging to this downstream manifestation of aging. Nor is it entirely clear how to
Article originally posted at