As Daniel Patrick Moynihan, an American sociologist, politician, and diplomat once said: “Everyone is entitled to his own opinion, but not his own facts”. And we wholeheartedly agree. A shared set of facts is the first step to building a better world with longevity for all. In that spirit, we are creating a series that covers 101 indisputable facts about ageing, health and longevity.
Mitochondria are essential cellular ‘organs’ (organelles), as they are responsible for converting nutrients into energy in the form of a molecule called ATP. Mitochondria were not always permanent residents in our cells – deep in their evolutionary past, they were separate organisms with their own DNA. Even today, some of that DNA remains within each mitochondrion rather than inside the nucleus where the rest of the cell’s genetic information resides. This mitochondrial DNA (mtDNA) contains the code for the proteins that mitochondria use to create ATP. Unfortunately, the mtDNA’s position within the mitochondria makes it vulnerable to damage by products of ATP production called free radicals.
Free radicals are highly reactive molecules that tend to damage proteins and DNA. Mitochondria are producing a low level of free radicals all of the time, and since mitochondrial DNA is stored within the mitochondria, it is particularly exposed to this source of damage, and is thought to mutate roughly 10 times faster than nuclear DNA. Cellular levels of antioxidants and free radical-scavengers, which protect against this damage, also decline with age. The result is that an increasing number of mitochondria become dysfunctional as we age, meaning that they do not produce ATP as efficiently as they should. These dysfunctional mitochondria are supposed to be destroyed by the cell in a recycling process called autophagy (also called mitophagy where mitochondria specifically are concerned). However, this process also becomes disrupted with age.
Mitochondrial dysfunction is thought to be one of the key processes that underpins ageing. Scientists have observed increased numbers of dysfunctional mitochondria in aged cells and have linked them to many diseases of ageing. ATP is an essential fuel for cells of all types, providing the energy needed for muscles to contract, for neurons to send electrical impulses, and for cells to control the concentration of ions inside their membranes. It’s possible that a deficit of ATP may be responsible for some aspects of ageing, particularly in tissues that demand a lot of energy like muscle. ATP is also required for processes that remove toxic proteins such as amyloid, thought to play a role in many age-associated diseases including Alzheimer’s.
Mitochondria are more than just power plants – they also provide important signals to the rest of the cell. These signals are important for orchestrating the disposal of damaged cellular components (autophagy) and cell suicide (apoptosis), which are both essential for keeping cells healthy while clearing out unhealthy ones. Dysfunctional mitochondria also deplete an important molecule called NAD+ (nicotinamide adenine dinucleotide), which is used in many processes that are vital to the cell such as the repair of damaged DNA, the recycling of damaged cell components, and the growth and division of existing mitochondria.
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