Longer genes may be a main cause, play role in Alzheimer’s

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  • Although aging is a natural part of life, everyone wants to slow this process down.
  • Recent studies show that certain lifestyle actions can help decelerate aging’s course.
  • Researchers from the Northwestern University Feinberg School of Medicine say that longer genes in the body might be a main cause of the body’s aging.
  • Scientists believe long genes may also play a role in the development of neurodegenerative diseases such as Alzheimer’s disease.

Everyone knows that aging is a natural part of life. However, that has not stopped humans wanting to know how to slow down the aging process.

Studies surrounding the Blue Zones where people consistently live over 100 years of age have brought some insights into how certain lifestyle actions can lead to healthy aging and a longer life.

Recent studies have examined other ways that may slow the aging process, including cutting calories, following a fasting-mimicking diet, and getting more physical activity.

“If we understand more about aging, it could help us to identify novel ways to monitor and improve health,” Thomas Stoeger, PhD, assistant professor of medicine in pulmonary and critical care at Northwestern University Feinberg School of Medicine, a member of the Potocsnak Longevity Institute, and co-corresponding author of a new report recently published in the journal Trends in Genetics, told Medical News Today.

“While multiple individual causes of aging are known, there is an outstanding need to understand why they all change the body in similar ways with age. This is the root of the problem,” Stoeger said.

In this report, Stoeger and his team from Northwestern University Feinberg School of Medicine report that long genes in the body — which are more susceptible to damage — might be a main cause of the body’s aging.

Additionally, researchers think that long genes may also play a role in the development of neurodegenerative diseases such as Alzheimer’s disease.

According to Stoeger, long genes are the template to build proteins that are large, generally because these proteins need a certain size to function properly.

“Many of those proteins are especially important for the functions of neurons. However, they are also important to other parts of the body,” Stoeger explained to MNT.

“The longer a gene, the more likely it is that it becomes damaged at least once. Singular damage to a gene can already prevent the body from building the protein templated by the gene. The longer the gene, the less likely it is that our bodies can build the proteins templated by these genes,” he continued.

Stoeger said that researchers do not yet fully understand all the consequences of damage to long genes.

“However, one consequence is that the body struggles and fails to produce the proteins encoded by the long genes. Thus, proteins essential for some of the body’s functions become selectively lost with age, according to the length of their genes,” he added.

This new report encompasses findings from four international research groups, which is reportedly the first to conclude that most aspects of biological aging are related to gene length.

The report also introduced a new term called gene length-dependent transcription decline (GLTD), which the scientists define as a “negative correlation between gene length and their expression in various cell types, species, and diseases.”

“Long genes that become less active with age may be the central cause of aging in our bodies. Our finding advances the field by identifying a single phenomenon that connects most existing knowledge about aging and makes this underlying phenomenon measurable. The regulation of genes is one of the most central processes of life, and our four studies explain why the activity of long genes in particular change in aging,” Stoeger says.

Researchers also state that long genes may play a role in the development of Alzheimer’s disease and other neurodegenerative diseases because expressed genes of neurons are normally long.

“The present study (opinion article) makes the connection between gene length in aging and Alzheimer’s Disease,” Stoeger said. “The idea for this manuscript stems from co-author Dr. Sourena Soheili-Nezhad, who made the initial observations on gene length in Alzheimer’s disease, alongside an unrelated study of Dr. Shahar Barbash and Prof. Thomas Sakmar.”

“Dr. Soheili-Nezhad did not seem surprised when he read about ongoing research of mine on aging, and didn’t need to convince me much that there could be a profound connection to his findings on Alzheimer’s disease,” he continued.

“Knowing about the importance of gene length in neurodegenerative disease makes it measurable. This allows for the design of experiments and interventions trying to increase the function of long genes,” he added.

After reviewing this report, David Merrill,MD,PhD, a geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center at Providence Saint John’s Health Center in Santa Monica, CA, told MNT that this study gives doctors a new way to discuss the aging process with patients.

“As we age, the longer, more complex genes have more spots on them that can become damaged. When they are damaged, the genes can no longer be transcribed into the RNA that then gets translated into the proteins that maintain normal cellular function. The damage comes from the wear and tear of living through processes like oxidative stress.”
— David Merrill, MD

“We can reduce oxidative stress on our cells and their genes by eating a healthy diet full of fresh whole foods like fruits and vegetables that are high in antioxidants. We can also participate in activities that promote DNA repair like exercise, intermittent fasting, or modest caloric restriction. Reducing stress and eating healthy fats like omega-3 also promotes DNA repair. Reducing or eliminating behaviors like smoking, drinking alcohol, or eating highly processed foods with added sugars also reduces the stress on our DNA,” Merrill said.

MNT also spoke with Dr. Rocco DiPaola, a neurologist and movement disorder specialist at Hackensack Meridian Neuroscience Institute at Jersey Shore University Medical Center in New Jersey, about this research.

DiPaola commented that this report helps explain the pathways that lead to aging and possibly neurodegenerative disorders.

“This becomes more important as our population ages and the resulting burden to patients, families, and society in general related to neurodegenerative disorders increases,” he continued. “Further research (should) determine if, in fact, GLTD is the main or one of multiple mechanisms of aging, and is it preventable.”

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