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   May 30

The brain’s ‘power cells’ shut down in old age

Researchers took cell samples from people ranging from newborns to age

They found that the mitochondria – tiny ‘power stations’ that fuel cells – from older donors were very different

Genes in the mitochondria that help with energy production were turned off and the mitochondria themselves were more damaged

Memory fades as people get older because their brain runs start running out of energy, like old car running out of gas, according to new research.

The key lies in mitochondria, tiny ‘power stations’ that convert our food into chemical energy our cells can use.

Aging does not affect their function in other parts of the body but it does affect function in the brain, said scientists from the Salk Institute for Biological Studies in La Jolla, .

The discovery sheds fresh light on a range of age-related brain diseases including Alzheimer’s and Parkinson’s – offering hope of better treatments.

For the study, the researchers took cell samples from people ranging from newborns to 89 years old.

They found few age-related changes. However, once the cells were directly converted into neurons, mitochondria from older donors were very different.

Mitochondrial genes related to energy production were turned off and the mitochondria in these ‘induced neurons’ (iNs) were less dense, more fragmented and generated less energy.


Alzheimer’s disease is a progressive brain disorder that slowly destroys memory, thinking skills and the ability to perform simple tasks.

It is the cause of 60 percent to 70 percent of cases of dementia.

The majority of people with Alzheimer’s are age 65 and older.

More than five million Americans have Alzheimer’s.

It is unknown what causes Alzheimer’s. Those who have the APOE gene are more likely to develop late-onset Alzheimer’s.

Signs and symptoms:

Stage of Alzheimer’s:

There is no known cure for Alzheimer’s, but experts suggest physical exercise, social interaction and adding brain boosting omega-3 fats to your diet to prevent or slowdown the onset of symptoms.

The researchers believe the reason the mitochondria of iNs were more damaged is that brain cells rely more heavily on mitochondria for their energy needs.

Co-corresponding author Dr Jerome Mertens, a stem cell biologist at the Salk Institute, used the analogy of a worn-out motor vehicle.

‘If you have an old car with a bad engine that sits in your garage every day, it doesn’t matter,’ he said.

‘But if you are commuting with that car, the engine becomes a big problem.’

This impaired energy production may explain why the brain is so prone to dementia and other illnesses over time.

Dr Mertens and his colleagues used a new method to discover that cells from older individuals had impaired mitochondria – and reduced energy production.

‘Most other methods use chemical stresses on cells to simulate aging,’ said senior author Professor Rusty Gage, of Salk’s Laboratory of Genetics.

‘Our system has the advantage of showing what happens to mitochondria that age naturally, within the human body.’

Previously, Professor Gage’s lab developed a technique to directly convert skin cells into induced neurons.

Most methods had relied upon an intermediary step, creating what are called induced pluripotent stem cells, which reset cellular markers of aging.

They can potentially produce any cell or tissue the body needs to repair itself.

But Professor Gage’s neurons (iNS) retained signs of aging – including changes to the nucleus, which contains the majority of the cell’s genetic material.

The latest study uncovered whether the mitochondria also retained hallmarks of aging during the conversion process.

They did this by creating neurons out of the skin cells collected from each donor and studying the mitochondria of every set in a variety of ways.

The researchers next want to begin to apply the technique to study age-related diseases, including Alzheimer’s and Parkinson’s.

By collecting skin cells from patients and creating iNs, the team can look at how mitochondria in neurons from patients with those diseases are different from mitochondria in neurons from older people without these illnesses.

Source: Daily Mail

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