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How Aging Affects Mitochondria in Brain Cells and Contributes to Age-Related Diseases

In recent years, it's become increasingly apparent that most of what we refer to as health and disease really links back to the function of your mitochondria — tiny organelles inside your cells that play an important role in the production of adenosine triphosphate (ATP), required for all biological functions. If your mitochondria are not functioning well, your risk for chronic degenerative diseases will radically increase. Not surprisingly, optimization of mitochondria is also vital for life extension strategies. 

Your brain, being the most energy-dependent organ (consuming up to 20 percent of the energy used by your entire body1), is therefore particularly susceptible to impaired energy production due to faulty mitochondria, and researchers now suggest this appears to be what makes the human brain susceptible to age-related diseases in the first place. As reported by Salk News:2

"Salk researchers used a new method to discover that cells from older individuals had impaired mitochondria — the power stations of cells — and reduced energy production. A better understanding of the effects of aging on mitochondria could reveal more about the link between mitochondrial dysfunction and age-related brain diseases such as Alzheimer's and Parkinson's."

Mitochondrial Dysfunction and Age-Related Brain Disease

The research3 in question, published in the May issue of Cell Reports, supports "a bioenergetic explanation for the high susceptibility of the brain to aging." With age, your mitochondria tend to decrease both in number and function, and this age-related dysfunction is caused by impaired ATP production and an increase in oxidative damage. According to the authors: 

"Mitochondrial dysfunction is characterized by the loss of the mitochondrial membrane potential, which is directly linked to a loss of energy generated through the electron transport chain that performs oxidative phosphorylation (OXPHOS); the failure of OXPHOS is believed to set the stage for the development of age-related disorders.

Interestingly, inherited mitochondrial diseases that can be caused by mutations in genes encoded on the nuclear DNA, which encodes the vast majority of mitochondrial genes, or in genes that are encoded in mtDNA are often associated with neurodegenerative phenotypes, indicating a particular vulnerability of brain neurons to mitochondrial defects.

Similarly, the human brain is an organ that is strongly affected by aging, and advanced age is by far the strongest risk factor for most neurodegenerative disorders."

While most investigative methods employ chemical stressors on cells to simulate cellular aging, the Salk group, led by Rusty Gage, a Salk Laboratory of Genetics professor, used a novel method previously developed by Gage that directly converts skin cells into neurons, referred to as "induced neurons" or iNs. These iNs allowed them to observe the effects of natural aging on mitochondria. 

Mitochondrial Genes Related to Energy Generation Are Turned Off in Older Individuals

For the featured study, the team collected skin cells from individuals ranging in age from newborn to 89, and then created iNs from each donor. They then studied the mitochondria within each set, using a variety of different methods. Interestingly, while the mitochondria in the skin cells showed few variations between age groups, once the cells were converted to neurons, significant differences emerged.

In the iNs of older individuals, mitochondrial genes related to energy generation were turned down. The mitochondria were also less dense and more fragmented, and generated much lower amounts of energy. The mitochondrial membrane potential was on average 43 percent lower in old iNs compared to young iNs. 

"Pretty much every area we looked at — functional, genetic and morphological — had defects," Jerome Mertens, a Salk staff scientist and co-corresponding study author said. The authors also noted that the differences in susceptibility to mitochondrial aging between various cell types appears to depend on the level of oxidative phosphorylation the cell in question performs, and that "the metabolic profile of neurons might render them particularly vulnerable to mitochondrial aging." As reported by Salk News:

"The researchers hypothesized that the reason the mitochondria of iNs were more impacted by aging than the mitochondria of skin cells was that neurons rely more heavily on mitochondria for their energy needs. 'If you have an old car with a bad engine that sits in your garage every day, it doesn't matter,' Mertens says. 'But if you're commuting with that car, the engine becomes a big problem.'

The finding shows how aging can impact organs differently throughout the body. The researchers next want to begin to apply their method to study age-related diseases, including Alzheimer's and Parkinson's. In the past, mitochondrial defects have been implicated in these diseases.

By collecting skin cells from patients and creating iNs, the team can look at how neuronal mitochondria from patients with those diseases are different from neuronal mitochondria from unaffected older individuals."

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