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Health November 2013

Aid for Age

Cells Breaking Bad: Aging DNA and You

By Tait Trussell

Dr. Belancio’s current studies in her lab are conducted to understand how L1 itself changes with aging. Also, she seeks to find out how the L1 can change the cell and the stability of its DNA because of aging.

Why is it that cancer attacks mainly the elderly?

One scientist, who studies why some cells suddenly go bad and lead to disease, does her work on what is probably the smallest size human element — the size of one’s DNA.

In case you’ve forgotten, DNA is deoxyribonucleic acid. It’s a material present in living organisms. It carries genetic information and is the main constituent of chromosomes. Everybody’s DNA is different.

Although this deals with cancer and seniors, if this sounds as if it will be too scientifically technical, you may want to stop here. I won’t warn you again. This article deals also with why people age differently.

The scientist who is seeking answers to these mysteries is Dr. Victoria Belanchio. She is professor of Cellular Biology at Tulane University School of Medicine’s Center for Aging.

Fragments of DNA are present in our genomes, the entirety representing about 40 percent of DNA — “are present in our genomes (our hereditary combination) in many copies because of their activity,” says Dr. Belancio. The red-headed, bespectacled professor says the L1 element (it stands for long interspersed element one) can change a cell in different ways. “The L1 element can amplify by inserting a copy of itself into a new position within the DNA or it can shuffle portions of the DNA as it inserts elsewhere.”

Since the mutagenesis (a process of changing a DNA) is random, these elements are known to cause a variety of human diseases, ranging from hemophilia (a medical condition where the blood won’t clot, causing severe bleeding) to cancer, depending on which gene they alter when they insert themselves.

Dr. Belancio’s current studies in her lab are conducted to understand how L1 itself changes with aging. Also, she seeks to find out how the L1 can change the cell and the stability of its DNA because of aging.

In the lab, the scientists can study L1 elements by using evaluations in tissue culture in which the L1 elements have a tag that generates a color when the L1 elements insert into the DNA.

Professor Belanchio tells us that “historically, the L1 elements have been considered to be DNA parasites.” They occupy a sizeable portion of our DNA. Speculation still swirls around whether their origin is from retroviruses (retroviruses are genes encoded RNA instead of DNA. RNA is an acid that, in some viruses, carries the genetic information.) Other scientists believe that we can’t get rid of L1, meaning our cells have to coexist with them. Understand, so far?

Historically, Belancio explains, the L1 elements are considered to be DNA parasites. They form a large part of our DNA, There is still speculation, she says, whether they come from retroviruses that integrated into our DNA. This speculation is because they share certain features with retroviruses.

She says there are two schools of thought in the scientific field, when it comes to L1 elements. Some researchers believe they have a function, which is why we have maintained them in our DNA. Still others believe we can’t get rid of L1, meaning our cells have to coexist with them.

The term “junk DNA” (parts of the genome which seems to be useless) have new meaning for Dr. Belancio. Instead of being of no consequence to normal cellular existence, L1 elements are now considered a burden which cells have to deal with.

On the flipside, L1 elements sometimes can generate new genes with new functions. What she seeks to answer is how the cells balance the good and bad associated with L1 expression.

“Can L1 be one of the contributors to natural aging and cancer that have not previously been considered? We have reported L1 expression in normal human cells that were previously anticipated to suppress the L1-associated damage; so we also want to know how much of this damage is occurring and whether there is a difference between different cell types.”

Understanding how the L1 elements contribute to age-related diseases is our first goal, she said. The long-term goal is to identify ways of preventing these diseases.

The immediate goal is to understand what controls L1 and how it can contribute to cancer and aging. “Then once we understand that we can think of strategies to inhibit its activity,” she explained.

 

Tait Trussell is an old guy and fourth-generation professional journalist who writes extensively about aging issues among a myriad of diverse topics.

Meet Tait