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Can we stay young and healthy longer by 'cleaning' our cells?

2022-05-02T04:00:21.911Z


A group of researchers wants to find out if boosting this natural process, known as autophagy, can curb the debilitating diseases of old age


Is it possible to intervene in the processes that cause our bodies and brains to malfunction as we age, thereby delaying the onset of age-related disorders, or even preventing them from developing altogether?

The legend of the mythical fountain of youth has enjoyed popularity for thousands of years.

The question of whether we can drink its waters has continued to haunt researchers working in the field of biological aging (known as senescence) since, in 1889, the French doctor Charles-Édouard Brown-Séquard injected extracts from testicles of animals.

After the treatment, the scientist stated that his mental and physical state had improved.

More information

“We are better off if we reduce calorie intake to 60%”

Nearly 150 years later, age-related disorders like Alzheimer's and heart disease have reached epidemic levels in the global North, and the quest for rejuvenation remains alluring.

Not surprisingly, this increase in disease is largely attributable to longer life expectancies.

People born in Europe today can reach 81.3 years, about 35 years more than those who came into the world at the end of the 19th century.

However, doctors agree that quality of life in old age has not kept pace with longevity.

Many of us spend years—sometimes decades—of old age living with physical or mental illnesses caused almost exclusively by the aging process.

We often lack treatments for the diseases of old age, the symptoms of which can be "very debilitating, sometimes devastating," according to Nektarios Tavernarakis, a bioscientist and professor at the University of Crete in Greece who studies aging, cell death, and neurodegeneration.

"Our goal has to stop being to live longer and move on to achieving a better quality of life in old age," says the researcher, who is also the main coordinator of the Macroautophagy and Necrotic Neurodegeneration in Old Age (MANNA) project. English), financed by the European Union.

Cellular detoxification

The goal of Tavernakis and his colleagues is to understand - and eventually remedy - the cellular causes of biological deterioration.

The benefits of prolonging one person's years of health will be felt throughout society.

Poor health in old age represents a huge and growing burden on our health and social systems.

Alzheimer's alone affects more than 4.9 million people in Europe, and diseases and disorders of the nervous system and brain cost the continent some 800 billion euros annually, according to 2010 figures.

The question is how scientists hope to solve the problem of physiological deterioration with so many seemingly unrelated disorders clamoring for their attention.

From the different types of cancer to diseases that attack the internal organs, the circulatory system and the nervous system, there is a whole series of ailments associated with aging.

Many pin their hopes on a biological process called autophagy (a term that means "eating oneself" in Greek).

Cells use autophagy to get rid of toxic material (mostly unnecessary or damaged components).

As we age, this basic housekeeping task becomes less efficient, leading to the accumulation of errors and malfunctions that trigger disease-causing inflammation and ultimately necrotic cell death (or necrosis).

We have a growing body of evidence that defective autophagy is the common denominator of many age-related disorders.

Necrosis contributes to the incidence of tumors, liver disease, stroke, heart disease, and age-related degenerative disorders such as Alzheimer's and Parkinson's.

"Our goal has to stop being to live longer and move on to achieving a better quality of life in old age"

Nektarios Tavernarakis, bioscientist and professor at the University of Crete

Research in this field is in its infancy, but a growing number of studies indicate that enhancing autophagy can extend cell survival and improve our prospects for good health.

Looking to the future, Linda Partridge, founding director of the Max Planck Institute for the Biology of Aging in Germany, says: “We see the possibility of developing a single pill that targets biological pathways that also influence autophagy.

The idea would be to have a polypill that tackles the underlying mechanisms that intervene in more than one age-related disease”.

“If we could attack these underlying aging processes, we might be able to slow down age-related degeneration and keep people healthier for longer.

This would take us to a different place than today, where diseases are treated one by one as they appear.

Partridge is the principal investigator of GeroProtect, a project funded by the European Union whose aim is to find a suitable drug for this “geroprotective” polypill.

"We are not trying to prolong life span, but rather to solve the problem of the increasingly long phase of poor health at the end of life," she explains.

Nektarios Tavernakis' MANNA project is focused on unraveling the connection between autophagy and age-related degeneration of the nervous system.

Much of the group's research is done on the worm

Caenorhabditis elegans

, which, perhaps surprisingly, has a nervous system very similar to that of humans.

During the first four years of the project, the team has discovered some of the key genes and molecular players involved in nerve cell necrosis.

Their work confirms that the long-term survival and preservation of neurons depends on a subtype of autophagy called mitophagy.

"We do not intend to prolong the duration of life, but to solve the problem of the increasingly long phase of ill health at the end of life"

Linda Partridge, founding director of the Max Planck Institute for the Biology of Aging in Germany

At its peak, the body uses mitophagy to eliminate mitochondria (the organelles that serve the cell to convert glucose - or simple sugar - into useful energy).

But with age, mitophagy slows down, and defective mitochondria begin to accumulate in nerve cells.

This accumulation is toxic, causing an inflammatory response that leads to cell deterioration and death.

This progressive loss of functional nerve cells is what causes the onset of neurodegenerative diseases.

"Our work on

C. elegans

and human brain tissue allows us to confirm that mitophagy is downregulated in Alzheimer's patients," explains Tavernakis.

The researcher adds that the efforts to decipher the precise mechanisms that influence the malfunction of mitophagy are still ongoing, but he trusts that in the end we will have complex gene therapies to replace the genetic sequences that accelerate necrosis with others that enhance autophagy healthy well into old age.

However, there are still many years to go before these therapies arrive.

Eat less, live more

A known way to induce autophagy is caloric restriction.

In experiments with worms, flies, mice, chimpanzees and humans, researchers have found that consuming less food or reducing an organism's meal times over the span of a day activates the cellular process.

In non-human species, dietary restriction has also been found to prolong life and reduce or delay the onset of age-related diseases.

Depending on the species, the most promising results show increases in life expectancy of between 50% and 300%.

There is also suggestive evidence that reduced dietary intake positively influences aging in primates, although the effects for humans are still debatable.

Why can it feel good to go hungry?

Simply because when an organism's diet is restricted, its cells stop receiving glucose and begin to consume their own discarded material in order to produce energy.

In other words, to sustain themselves, cells are forced to enter a state of autophagy that detoxifies them.

disease prevention

The problem with diet restriction is that people generally don't like it, and in humans, any attempt to reduce food intake is usually short-lived.

So when it comes to boosting autophagy, pharmacological interventions are a more realistic alternative (although Partridge insists that overactivating the cleaning process can also be problematic, as it can cause cells to destroy their contents at too fast a rate) ).

A few promising drugs have already been found.

The main ones are urolithin A (produced by certain intestinal bacteria after being fed on ellagitannins, found in pomegranates, strawberries, raspberries and walnuts) and rapamycin (a natural antifungal secreted by soil bacteria).

These two compounds are known to participate in the upregulation of autophagy.

In addition, they have been found to prolong life in mice, worms, and fruit flies.

Its geroprotective properties will soon be tested in human clinical trials.

Partridge, who has studied the underlying mechanisms responsible for rapamycin's efficacy in relaunching autophagy in animal models, is confident that the results of the human trials will bring his team closer to developing the revolutionary polypill.

"Eventually, we could have a drug that is taken more or less like statins (for cholesterol) or pills to reduce blood pressure are taken today," he says.

“Medications that are taken over a long period of time to prevent disease long before it appears.”

The research described in this article was financed with EU funds.

Article originally published in

Horizon

, the Research and Innovation magazine of the European Union.

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Source: elparis

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