Mitochondria In Geriatrics

A mitochondrion acts as a powerplant of a cell. They process food and oxygen to make carbon dioxide, water and Adenosine triphosphate (ATP). Carbon dioxide and water we exhale, but ATP is essential to cellular function acting as a "currency" for energy. See this for an overview of ATP.

As our mitochondria age, they collect damage, and mutation just like the rest of our cells. This damage is not, in any meaningful way, different to mitochondrial disease, other than a public perception that because we're old, and it's a normal part of ageing, it doesn't matter.

Given their role, as they begin to gather mutation, and collect damage, they become less and less able to do their jobs, again, in the same way as in mitochondrial diseases in children. The positive feedback loop occurs as damaged mitochondria are less able to do their job, which leads to higher levels of toxins and oxidate damage, which leads to greater mitochondrial damage, which leaves mitochondria less able to do their job, etc.*

In older patients, several changes occur to mitochondria including a decrease in activity of enzymatic proteins of the respiratory chain and deletions and mutations in mtDNA cause greater oxidative stress (adding to the above positive feedback loop).

Despite this, it's still uncertain if mitochondrial damage is a cause, or a symptom of ageing. Either way, however, it does speed up the process, and leads to death.

Diseases linked to mitochondria at a geriatric age include, but are certainly not limited to, dementia, parkinsons, alzheimers, heart disease, stroke, diabetes, and normal, everyday cell death, which kills us all.