Scientists have long pondered why people age.

That is, until last December, when Northwestern researchers published a study describing how gene length correlates to aging, opening the door to new interventions and studies.

All cells have both short and long genes, but as organisms age, shorter genes become more and more active, according to the study.

Principal investigator Thomas Stoeger said it is significant how universal the process is across all animals.

“It’s kind of a shared principle about aging that is much older than humans,” Stoeger said.

Senior author and McCormick Prof. Luis Amaral said the discovery provides a “unifying picture” of the aging process. He said while everyone lives a different life, they age in the same way.

Amaral said cells, like factories, balance everything they produce, and as cells age, the imbalances develop. As injuries accumulate, the body expends more energy repairing itself, he said. As a result, the body takes longer to heal small things, such as cuts, he said.

The imbalance begins for humans relatively early, before they turn 40 years old, Stoeger said.

Amaral attributed the association between gene length and aging as Stoeger’s “brilliant insight.”

“It’s like one of those crime mysteries in which suddenly all the clues just come together,” Amaral said. “And you say ‘Yes, this is the culprit.’”

He said the discovery combined other scientists’ studies and research. Other research papers have analyzed different parts of the aging process.

Stoeger said discovering how the commonalities behind aging could change the way people think about aging and aging-related disease. It would allow for scientists to work not just with the specific diseases, but with the process of aging itself.

Biology Prof. Richard Morimoto said understanding aging is important because every human being worries about it.

“The only things that don’t age are physical materials,” Morimoto said. “Atoms stay atoms forever, but everything that we know of — plant or animal — ages, and therefore brings up one of the most fascinating questions: How, when and why does biology age?”

Amaral said the paper allows researchers to pursue more questions on why and where these cellular failures happen.

Morimoto asked the question: Does this mean aging can be reversed? Would there be consequences if they tried to reverse it?

Meanwhile, Stoeger said he has a simpler approach as to why he believes studying lesser-known genes matters: research bias.

He said only a small subset of genes are being researched. For example, half of the genes that have a strong correlation to Alzheimer’s disease have never been studied by a small laboratory.

“For me, the big problem is breaking this pattern of historically acquired biases,” he said. “And my other research is about these biases … You can use understanding of those biases to arrive at novel biological research.”

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