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NEWS & RESEARCH


LOSS OF EPIGENETIC INFORMATION CAN DRIVE AGING, RESTORATION CAN REVERSE IT


STUDY IN MICE IMPLICATES CHANGES TO WAY DNA IS ORGANIZED, REGULATED RATHER THAN
CHANGES TO GENETIC CODE ITSELF

By STEPHANIE DUTCHEN January 12, 2023 Research

8 min read

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Genetics professor David Sinclair explains how changes to DNA organization and
regulation can accelerate or reverse signs of aging in mice. Video: Rick Groleau
and Bruce Walker


An international study 13 years in the making demonstrates for the first time
that degradation in the way DNA is organized and regulated — known as
epigenetics — can drive aging in an organism, independently of changes to the
genetic code itself.

The work shows that a breakdown in epigenetic information causes mice to age and
that restoring the integrity of the epigenome reverses those signs of aging.

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Findings are published online Jan. 12 in Cell.

“We believe ours is the first study to show epigenetic change as a primary
driver of aging in mammals,” said the paper’s senior author, David Sinclair,
professor of genetics in the Blavatnik Institute at Harvard Medical School and
co-director of the Paul F. Glenn Center for Biology of Aging Research.

The team’s extensive series of experiments provide long-awaited confirmation
that DNA changes are not the only, or even the main, cause of aging. Rather, the
findings show, chemical and structural changes to chromatin — the complex of DNA
and proteins that forms chromosomes — fuel aging without altering the genetic
code itself.


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“We expect the findings will transform the way we view the process of aging and
the way we approach the treatment of diseases associated with aging,” said
co-first author Jae-Hyun Yang, research fellow in genetics in the Sinclair lab.

The authors say that because it’s easier to manipulate the molecules that
control epigenetic processes than to reverse DNA mutations, the work points to
new avenues that focus on epigenetics rather than genetics to prevent or treat
age-related damage.

First, the results need to be replicated in larger mammals and in humans.
Studies in nonhuman primates are currently underway.

“We hope these results are seen as a turning point in our ability to control
aging,” said Sinclair. “This is the first study showing that we can have precise
control of the biological age of a complex animal; that we can drive it forwards
and backwards at will.”


BEYOND MUTATIONS

Perhaps the most burning question for those who study aging is what causes it.

For decades, a reigning theory in the field was that aging arises from an
accumulation of changes to DNA, primarily genetic mutations, which over time
prevent more and more genes from functioning properly. These malfunctions, in
turn, cause cells to lose their identity, so that tissues and organs break down,
leading to disease and, ultimately, death.

In recent years, however, studies have increasingly hinted that there’s more to
the story.

For instance, some researchers found that some people and mice with high
mutation rates don’t show signs of premature aging. Others observed that many
types of aged cells have few or no mutations.

Researchers started wondering what else works with or instead of DNA changes to
cause aging. A list of possible culprits grew. Among them were epigenetic
changes.

A component of epigenetics is the physical structures such as histones that
bundle DNA into tightly compacted chromatin and unspool portions of that DNA
when needed. Genes are inaccessible when they’re bundled up but available to be
copied and used to produce proteins when they’re unspooled. Thus, epigenetic
factors regulate which genes are active or inactive in any given cell at any
given time.

By acting as a toggle for gene activity, these epigenetic molecules help define
cell type and function. Since each cell in an organism has basically the same
DNA, it’s the on-off switching of particular genes that differentiates a nerve
cell from a muscle cell from a lung cell.

“Epigenetics is like a cell’s operating system, telling it how to use the same
genetic material differently,” said Yang, who is co-first author with Motoshi
Hayano, a former postdoctoral fellow in the Sinclair lab who is now at Keio
University School of Medicine in Tokyo.

In the late 1990s and early 2000s, Sinclair’s lab and others showed in yeast and
mammals that epigenetic changes accompany aging. Yet they couldn’t tell whether
these changes drove aging or were a consequence of it.

It wasn’t until the current study that Sinclair’s team was able to disentangle
epigenetic from genetic changes and confirm that a breakdown in epigenetic
information does, in fact, contribute to aging in mice.


ICE MICE

The team’s main experiment involved creating temporary, fast-healing cuts in the
DNA of lab mice.

These breaks mimicked the low-grade, ongoing breaks in chromosomes that
mammalian cells experience every day in response to things like breathing,
exposure to sunlight and cosmic rays, and contact with certain chemicals.

In the study, to test whether aging results from this process, the researchers
sped the number of breaks to simulate life on fast-forward.

The team also ensured that most of the breaks were not made within the coding
regions of the mice’s DNA — the segments that make up genes. This prevented the
animals’ genes from developing mutations. Instead, the breaks altered the way
DNA is folded.

Sinclair and colleagues called their system ICE, short for inducible changes to
the epigenome.

At first, epigenetic factors paused their normal job of regulating genes and
moved to the DNA breaks to coordinate repairs. Afterward, the factors returned
to their original locations.

But as time passed, things changed. The researchers noticed that these factors
got “distracted” and did not return home after repairing breaks. The epigenome
grew disorganized and began to lose its original information. Chromatin got
condensed and unspooled in the wrong patterns, a hallmark of epigenetic
malfunction.

As the mice lost their youthful epigenetic function, they began to look and act
old. The researchers saw a rise in biomarkers that indicate aging. Cells lost
their identities as, for example, muscle or skin cells. Tissue function
faltered. Organs failed.

The team used a recent tool developed by Sinclair’s lab to measure how old the
mice were, not chronologically, in days or months, but “biologically,” based on
how many sites across the genome lost the methyl groups normally attached to
them. Compared to untreated mice born at the same time, the ICE mice had aged
significantly more.


YOUNG AGAIN

Next, the researchers gave the mice a gene therapy that reversed the epigenetic
changes they’d caused.

“It’s like rebooting a malfunctioning computer,” said Sinclair.

The therapy delivered a trio of genes — Oct4, Sox2, and Klf4, together named OSK
— that are active in stem cells and can help rewind mature cells to an earlier
state. (Sinclair’s lab used this cocktail to restore sight in blind mice in
2020.)

The ICE mice’s organs and tissues resumed a youthful state.

The therapy “set in motion an epigenetic program that led cells to restore the
epigenetic information they had when they were young,” said Sinclair. “It’s a
permanent reset.”

How exactly OSK treatment achieved that remains unclear.

At this stage, Sinclair says the discovery supports the hypothesis that
mammalian cells maintain a kind of backup copy of epigenetic software that, when
accessed, can allow an aged, epigenetically scrambled cell to reboot into a
youthful, healthy state.

For now, the extensive experiments led the team to conclude that “by
manipulating the epigenome, aging can be driven forwards and backwards,” said
Yang.


FROM HERE

The ICE method offers researchers a new way to explore the role of epigenetics
in aging and other biological processes.

Because signs of aging developed in the ICE mice after only six months rather
than toward the end of the average mouse life span of two and a half years, the
approach also saves time and money for researchers studying aging.

Researchers can also look beyond OSK gene therapy in exploring how lost
epigenetic information might be restored in aged organisms.

“There are other ways to manipulate the epigenome, like drugs and small molecule
chemicals that induce gentle stress,” said Yang. “This work opens a door for
applying those other methods to rejuvenate cells and tissues.”

Sinclair hopes the work inspires other scientists to study how to control aging
to prevent and eliminate age-related diseases and conditions in humans, such as
cardiovascular disease, type 2 diabetes, neurodegeneration, and frailty.

“These are all manifestations of aging that we’ve been trying to treat with
medicines when they arise, which is almost too late,” he said.

The goal would be to address the root causes of aging to extend human health
span: the number of years that a person remains not just alive but well.

Medical applications are a long way off and will take extensive experiments in
multiple cell and animal models. But, Sinclair said, scientists should think big
and keep trying in order to achieve such dreams.

“We’re talking about taking someone who’s old or sick and making their whole
body or a specific organ young again, so the disease goes away,” he said. “It’s
a big idea. It’s not how we typically do medicine.”


 * LONG TIME COMING
   
   The study marks the culmination of 10 years of Yang’s career as a
   postdoctoral researcher.
   
   But there were moments along the way when he thought he’d never see the work
   completed.
   
   As the scope expanded year after year, with colleagues and critics urging
   Yang to add more experiments and incorporate new technologies, the project
   often felt overwhelming. Yang sometimes listened to those who asked whether
   it was all worth it. At one point he drafted an email to Sinclair saying he
   wanted to quit the project.
   
   “Luckily,” said Sinclair, “he didn’t send it.”
   
   The problem wasn’t Yang’s skills or dedication. Rather, the work was the most
   ambitious ever attempted in the lab. Sinclair thinks it may represent one of
   the hardest projects undertaken in science in recent years.
   
   “You don’t get many chances in life to do a project like this,” he said. “It
   took an incredible amount of mental and physical labor to get to this point.
   Jae and the team demonstrated so much resilience as we got rejected and
   re-reviewed and did six more years of experiments until we ended up with a
   body of work that answers one of the most important questions in biology. I’m
   really proud of the team.”
   
   Seeing the findings published at long last not only offers professional
   satisfaction but also feels poignant on a personal level, Sinclair said.
   
   “This project began when I was 39. I’m now 53,” he said. “A lot has happened
   in those years. We’re older. Our families and friends have changed. People on
   the project have died. It’s more than just a paper for us; it’s a major part
   of our lives.”
   
   “There’s a lot of emotion in this,” he continued. “I feel like some of my
   soul is in there.”
   
   For his part, Yang hopes to now become a principal investigator in Korea,
   where he grew up.
   
   “I’m very happy to have answered one of the long-standing questions in the
   field,” he said. “I’m really looking forward to seeing the impact.” 


AUTHORSHIP, FUNDING, DISCLOSURES

Additional authors on the study are Patrick Griffin, João Amorim, Michael
Bonkowski, John Apostolides, Elias Salfati, Marco Blanchette, Elizabeth Munding,
Mital Bhakta, Yap Ching Chew, Wei Guo, Xiaojing Yang, Sun Maybury-Lewis, Xiao
Tian, Jaime Ross, Giuseppe Coppotelli, Margarita Meer, Ryan Rogers-Hammond,
Daniel Vera, Yuancheng Lu, Jeffrey Pippin, Michael Creswell, Zhixun Dou, Caiyue
Xu, Sarah Mitchell, Abhirup Das, Brendan O’Connell, Sachin Thakur, Alice Kane,
Qiao Su, Yasuaki Mohri, Emi Nishimura, Laura Schaevitz, Neha Garg, Ana-Maria
Balta, Meghan Rego, Meredith Gregory-Ksander, Tatjana Jakobs, Lei Zhong, Hiroko
Wakimoto, Jihad Andari, Dirk Grimm, Raul Mostoslavsky, Amy Wagers, Kazuo
Tsubota, Stephen Bonasera, Carlos Palmeira, Jonathan Seidman, Christine Seidman,
Norman Wolf, Jill Kreiling, John Sedivy, George Murphy, Richard Green, Benjamin
Garcia, Shelley Berger, Philipp Oberdoerffer, Stuart Shankland, Vadim Gladyshev,
Bruce Ksander, Andreas Pfenning, and Luis Rajman.

This work was supported by the National Institutes of Health (grants
R01AG019719, R37AG028730, R01EY019703, R01DK056799-10, R01DK056799-12,
R01DK097598-01A1, T32AG023480, and K99AG055683), Glenn Foundation for Medical
Research, Glenn/AFAR Research Grants for Junior Faculty, National Research
Foundation of Korea (2012R1A6A3A03040476), Human Frontier Science Program
(LT000680/2014-L), JSPS KAKENHI (17K13228, 19K16619 and 19H05269), Uehara
Memorial Foundation, and St. Vincent de Paul Foundation. The authors also
acknowledge the Dalio Foundation, Susan and Duane Hoff, the VoLo Foundation, and
Edward Schulak.

Sinclair is a consultant to, inventor of patents licensed to, and in some cases
board member and investor of MetroBiotech, Cohbar, InsideTracker, Zymo, EdenRoc
Sciences and affiliates including Cantata/Dovetail, Life Biosciences and
affiliates, Segterra, and Galilei Biosciences, Immetas, Animal Biosciences, and
Tally Health. He is also an inventor on patent applications licensed to Bayer
Crops, Merck KGaA, and Elysium Health. Details available here. Munding,
Blanchette, and Bhakta are employees of Dovetail Genomics. Chew, Guo, and Yang
are employees of Zymo Research Corporation. Wagers is a consultant to Frequency
Therapeutics and a co-founder of Elevian. Schaevitz was an employee of Vium. Lu
and Rajman are equity owners of Life Biosciences. Vera and Bonkowski were
advisors to Liberty Biosecurity. All other authors declare no competing
interests.

The authors dedicated their publication to the memory of co-authors Bonkowski
and Wolf and supporter Paul F. Glenn.


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WHY LOSS OF SMELL CAN PERSIST AFTER COVID-19

December 21, 2022
Research suggests that long-term smell loss is linked to an ongoing immune
response in the nose


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