Harnessing Your Gene System: Has The Key To Stopping Aging Been Discovered?

Groundbreaking research has uncovered a mechanism that could explain why we age and why brain diseases like Alzheimer's and Parkinson’s develop. It opens a whole new era of investigation into aging that currently doesn’t exist.

The new finding has the potential to not only slow aging but also reverse it. We're talking about a genetic discovery that goes beyond a single gene to a system made up of tens of thousands of genes.

What Is Your Gene System?

Scientists have traditionally believed many complex biological phenomena are attributable to a single or small number of genes. But this narrow approach can’t explain the multiple genetic changes that take place with aging.

A new concept being explored is to look at genes as a system, at the entirety of the 20,000 protein-coding genes in a human cell.

This systems-wide approach has borne fruit by uncovering a previously unknown mechanism that may be the key driver of aging. The new finding could lead to interventions that slow the pace of — or even reverse — aging.

Early Findings In Animals Reveal a Big Discovery

Scientists at Northwestern University examined multiple samples of different tissues from animals and human donors. Starting with mice, rats, and killifish samples at different ages across the lifespan, they noticed the average length of genes shifted, with longer genes linked to longer lifespans and shorter genes linked to shorter lifespans. Even starting early in life, short genes became more active, and long genes became less so, with the process becoming more pronounced with age.[1]

Thomas Stoeger, who led the research team, said: “The changes in the activity of genes are very, very small, and these small changes involve thousands of genes. We found this change was consistent across different tissues and in different animals. We found it almost everywhere.

“I find it very elegant that a single, relatively concise principle seems to account for nearly all of the changes in activity of genes that happen in animals as they age.[2]

When the scientists turned their attention to human samples, they found the same impact on aging as they did in animal models.

Long Genes Impact The Way You Age

They looked at changes in human genes from age 30 until death. Measurable changes in gene activity according to gene length were noticeable by the time humans reached middle age.

Commenting on their findings, senior scientist Luís Amaral said: “The result for humans is very strong because we have more samples for humans than for other animals.

“It was also interesting because all the mice we studied are genetically identical, the same gender and raised in the same laboratory conditions, but the humans are all different. They all died from different causes and at different ages. We analyzed samples from men and women separately and found the same pattern.”

Professor Stoeger believes “long genes that become less active with age may be the central cause of aging in our bodies.”[3]

It’s important to note that long genes are not the same thing as long telomeres.

Longer Genes vs. Longer Telomeres

You may recall that telomeres are the end caps of chromosomes. To get scientific, they are repetitive nucleotide sequences at the ends of chromosomes. They protect the ends of chromosomes from deterioration or fusion with other chromosomes. Telomeres shorten with each cell division, which is associated with aging and cellular senescence.

On the other hand, long genes refer to genes with a larger sequence length, meaning they contain more base pairs. From a scientific standpoint, they code for proteins or RNA molecules and include both coding (exons) and non-coding (introns) regions.

The length of a gene can influence its regulation—which is important in disease prevention-- and the complexity of the protein it encodes. Professor Amaral explains how gene length is related to aging. It’s due to a lack of homeostasis or balance.

Imbalanced Proteins Stress The Body

“The imbalance of genes causes aging because cells and organisms work to remain balanced — what physicians denote as homeostasis,” he said.

“Imagine a waiter carrying a big tray. That tray needs to have everything balanced. If the tray is not balanced, then the waiter needs to put in extra effort to fight the imbalance. If the balance in the activity of short and long genes shifts in an organism, the same thing happens. It’s like aging is this subtle imbalance, away from equilibrium. Small changes in genes do not seem like a big deal, but these subtle changes are bearing down on you, requiring more effort.”

For a cell to achieve homeostasis, several small proteins from short genes and large proteins from long genes are needed. Problems occur when that balance gets out of whack.

But why does this imbalance occur?

Long Genes Have Greater Damage Potential

It’s simply that long genes have more potential sites that could be damaged. The longer the gene, the more likely it is to have at least one site of DNA damage to prevent the gene’s activation.[4]

Certain activities that accelerate aging also decrease the activity of long genes. These include smoking, alcohol, excess free radicals (oxidative stress), and UV radiation from the sun. Calorie restriction, which slows aging, increases the activity of long genes.

Their findings also provide an explanation for neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease.

Long Genes And Your Memory

The brain is chock-full of long genes. The idea that the trigger of aging is a physical phenomenon related to the length of genes and not to the specific genes involved or the function of those genes is novel.

These findings, the scientists suggest, help explain how neurodegenerative diseases develop because many of the genes/proteins involved in brain loss during aging and linked with brain diseases are exceptionally long.

Thomas Stoeger explained, “Our findings help us rethink causes of neurodegenerative diseases such as Alzheimer’s disease. Because genes with neural function are unusually long, we hypothesize that with decreased activity of long genes, cells fail to produce sufficient biomaterials to maintain neural function properly.”

Such findings make him optimistic about the future because “if we would find a way to slow down the phenomena we have observed, maybe things aren’t that irreversible anymore.”