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Sanford Burnham Prebys and Salk co-organize third annual La Jolla Aging Meeting

AuthorMonica May
Date

April 11, 2019

Malene Hansen, PhD, and Peter Adams, PhD; and Salk’s Jan Karlseder, PhD

“Excellent presentation!”
“We should connect—we have more samples coming soon.” 
“Feel free to reach out, we’re looking to partner so I’d love to hear more about your research.”

These exchanges, overheard at the 3rd annual La Jolla Aging Meeting held on March 29, 2019, at the Salk Institute, illustrate the importance of uniting scientists focused on a common goal: In this case, uncovering the root causes of aging. 

As in previous years, the 2019 meeting was co-organized by Sanford Burnham Prebys’ Malene Hansen, PhD, and Peter Adams, PhD; and Salk’s Jan Karlseder, PhD A key goal of the event is to feature research by local scientists studying the molecular mechanisms of aging, while fostering connections and building relationships that advance new discoveries. More than 200 researchers, primarily from the San Diego area, attended the meeting. 

Aging is the main risk factor for many of the serious diseases our society faces today, including cancer, heart disease and Alzheimer’s. As the U.S. population grows older due to the natural aging of the Baby-Boomer generation, the need to understand the underlying causes of aging becomes more urgent. The number of Americans who are age 65 or older is projected to double from nearly 48 million in 2015 to more than 90 million in 2060, according to the United States Census Bureau. 

The diversity of presentations given—from the role of supportive brain cells called astrocytes and cellular recycling (autophagy) to long-lived proteins in mitochondria (the cell’s power generator)—reflects the complexity of the field. A poster session was also held during the symposium, providing an opportunity for up-and-coming scientists to share their recent data. 

La Jolla Aging Meeting tweet

For scientists new to the area, the meeting provided a key opportunity to build relationships.

“It’s unlikely there will be any single factor responsible for aging,” says Matt Kaeberlein, PhD, professor at the University of Washington and the symposium’s keynote speaker. “I am encouraged to see so many people interested in diverse aspects of aging biology at this symposium. By advancing each of these distinct research areas, and working together, we will make progress in understanding the underlying aging process.”

The full list of speakers follows. Make sure to save the date for next year’s meeting, which will be held on March 27, 2020. 

  • Matt Kaeberlein, PhD, University of Washington (keynote) – New insights into mechanisms by which mTOR modulates metabolism, mitochondrial disease and aging
  • Isabel Salas, PhD, Allen lab, Salk – Astrocytes in aging and Alzheimer’s disease
  • David Sala Cano, PhD, Sacco lab, Sanford Burnham Prebys – The Stat3-Fam3a axis regulates skeletal muscle regenerative potential
  • Tina Wang, Ideker lab, University of California, San Diego – A conserved epigenetic progression aligns dog and human age
  • Rigo Cintron-Colon, Conti lab, Scripps Research – Identifying the molecules that regulate temperature during calorie restriction
  • Nan Hao, PhD, University of California, San Diego – Programmed fate bifurcation during cellular aging
  • Shefali Krishna, PhD, Hetzer lab, Salk – Long-lived proteins in the mitochondria and their role in aging
  • Sal Loguercio, PhD, Balch lab, Scripps Research – Tracking aging with spatial profiling
  • Alva Sainz, Shadel lab, Salk – Cytoplasmic mtDNA-mediated inflammatory signaling in cellular aging
  • Anthony Molina, PhD, University of California, San Diego – Mitochondrial bioenergetics and healthy aging: Advancing precision healthcare for older adults
  • Alice Chen, Cravatt lab, Scripps Research – Pharmacological convergence reveals a lipid pathway that regulates C. elegans lifespan
  • Robert Radford, PhD, Karlseder lab, Salk – TIN2: Communicating telomere status to mitochondria in aging
  • Jose Nieto-Torres, PhD, Hansen lab, Sanford Burnham Prebys – Regulating cellular recycling: role of LC3B phosphorylation in vesicle transport

Prizes for the best poster presentations were awarded to the following scientists: 

  • Hsin-Kai Liao, PhD, Juan Carlos Izpisua Belmonte’s lab, Salk  
  • Yongzhi Yang, PhD, Malene Hansen’s lab, Sanford Burnham Prebys
  • Tai Chalamarit, Sandra Encalada’s lab, Scripps Research 

Thank you to our generous sponsor, the Glenn Foundation for Medical Research, and to NanoString for donating the prizes received by the poster presenters.  

Interested in keeping up with our latest discoveries, upcoming events and more? Subscribe to our monthly newsletter, Discoveries.
 

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The slow, silent process of “inflammaging” might kill you

AuthorSusan Gammon
Date

October 5, 2017

Huaxi Xu, PhD

You may recall from biology classes that most DNA is located in the nucleus, the cell’s command center that dictates cell growth, maturation, division and even cell death.  But occasionally, in aging cells that stop growing and dividing (senescent cells), bits of DNA pinch off and accumulate in the cytoplasm.  Although this may seem like an innocent act, cytoplasmic DNA actually triggers an inflammatory path that contributes to many diseases linked with aging.

“We are studying the mechanics of “inflammaging,” says Peter Adams, PhD, professor at SBP.  “The term refers to the pervasive, chronic inflammation that occurs in aging tissue. Understanding how inflammation occurs in aging tissue opens new avenues to treat a variety of age-related diseases such as rheumatoid arthritis, liver disease, atherosclerosis, muscle wasting (sarcopenia), and even cancer.”

Adams’ most recent study, a collaboration with Shelley Berger, PhD, professor at University of Pennsylvania, studied senescent cells to figure out how cytoplasmic DNA activates inflammation.  Senescent cells can be long-lived and accumulate in aged and damaged organs, attracting inflammatory cells that promote tissue damage.

Their new research, published in Nature, is the first to describe how in senescent cells, cytoplasmic DNA fragments activate the cGAS-STING pathway, a component of the immune system that leads to the secretion of pro-inflammatory cytokines.  

“Pro-inflammatory cytokines, such as interferon and tumor necrosis factor (TNF) promote inflammation, which can be a good thing when you need it,” explains Adams.  “Acute inflammation, for example, is a natural, healthy process that attracts and activates immune cells to heal wounds and fight infections.  And in the right circumstances, when our immune system recognizes cancer cells as foreign, these cytokines can activate powerful anti-tumor immune responses.

“But chronic, uncontrolled inflammation is a potentially harmful process.  It can lead to the destruction of tissue, and a list of diseases that range from skin conditions like psoriasis to deadly liver cancer.  So the inflammatory process must be tightly regulated to avoid excessive tissue damage and spillover to normal tissue—and these risks increase with age.

“Now that we understand how cytoplasmic DNA leads to chronic inflammation in senescent cells—through the cGAS-STING pathway—we have the opportunity to think about therapeutic strategies to intervene to delay or prevent “inflammaging” related diseases.

DOI: 10.1038/nature24050

Related: Cancer biology: Genome jail-break triggers lockdown (Nature Magazine)

 

 

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Slowing down the “aging clock”

AuthorJessica Moore
Date

April 14, 2017

old man walking across clock

What if it were possible to slow down the clock on aging? There may indeed be such a clock in all your cells. New research from the laboratory of Peter Adams, PhD, professor at Sanford Burnham Prebys Medical Discovery Institute (SBP), provides further evidence that the epigenome—the pattern of chemical tags across our chromosomes that help determine which genes can be read—is the key to aging.

“We found that conditions or treatments that extend lifespan make the epigenome of an old animal look like that of a much younger one,” says Adams, senior author of one of a pair of studies in Genome Biology. “In other words, the ‘epigenetic clock’ can be slowed. That suggests that to help people stay healthy longer and lower their risk of diseases like Alzheimer’s, cancer, and atherosclerosis, we should find molecules that do the same thing.”

Adams’ studies, performed in collaboration with the lab of Trey Ideker, PhD, professor at UC San Diego, build on previous findings in humans. Ideker and subsequently other teams of scientists had identified the genomic sites at which the presence or absence of a chemical tag correlates with age, and created an algorithm to tell a person’s age within two or three years by analyzing all those sites. This epigenetic clock speeds up in people with diseases that lead to earlier onset of aging-associated problems, such as obesity or HIV infection, or who have survived severe psychological stress in childhood.

Adams’ and Ideker’s teams showed that longevity-conferring interventions have the opposite effect—they put a brake on age-associated epigenetic changes. To make that discovery, they compared the epigenomes of normal mice to those of mice in which aging was slowed by three strategies that are all well known to extend the mouse lifespan: a longevity mutation (Prop1df/df, which also causes dwarfism), caloric restriction (reducing dietary intake significantly, but not enough to harm the mice), and rapamycin, a drug with multiple effects on metabolism and the immune system.

“To show that longer life correlates with slower epigenetic aging, we first had to delineate the mouse epigenetic clock,” adds Adams. “That provides us with a very useful tool. Now we can do experiments to find out whether epigenetic changes actually drive aging. For example, we can compare animals with slow and fast epigenetic clocks to see if the ones that age slower stay healthier as they age.

“And we can investigate how the epigenetic clock “ticks”—what cellular processes cause these changes over time? The answers to that question could identify targets for anti-aging medicines.”

Institute News

Your cells don’t lie (about your age)

AuthorJessica Moore
Date

February 23, 2017

older people jumping on the beach

Many scientists are searching for drugs that combat aging, not just to extend human lifespan, but to stay healthier longer, too.

One potential target for future anti-aging treatments are cells that have become stagnant—that can no longer replicate themselves. These cells, termed senescent, are found all over the body and appear to contribute to the breakdown of various organs over time, and to aging-related diseases ranging from cataracts to type 2 diabetes and maybe even Parkinson’s and Alzheimer’s.

Studying the role of senescent cells in aging tissue—and eventually, assessing whether reducing their numbers can slow aging—could become much easier thanks to a new study co-authored by Andrei Osterman, PhD The research, published in the Proceedings of the National Academy of Sciences, identifies a specific, measurable marker of senescent cells.

“We found that an oxidized form of vimentin, a protein that’s normally found inside cells as part of the cytoskeleton, is present on the surface of senescent cells, but no other kinds of cells,” Osterman says. “This discovery may lead to the development of tests to monitor aging-related decline in patients, as we found that levels of oxidized vimentin are elevated in the blood of mice that are genetically altered to age rapidly.”

Part of the new study, a continuing collaboration between Osterman and the Roswell Park Cancer Institute, involved analyzing antibodies that all recognize senescent cells in the same way.

Osterman adds, “A major part of the credit for identifying oxidized vimentin as the molecule those antibodies recognize goes to SBP’s proteomics core facility.

“We think that antibodies against senescent cells are produced throughout human life. It’s possible that as we age, our immune system slows down and stops producing antibodies that clear senescent cells from our bodies. Maybe boosting that immune function would be a way to decelerate aging.”

Several contributors to the study are affiliated with Everon Biosciences, a company that aims to create anti-aging medicines.

Institute News

An “Odd” gene affects aging of the heart

AuthorJessica Moore
Date

February 1, 2017

hands holding heart

As we get older, our hearts change in ways that make it harder for them to pump blood. They become stiffer, less efficient at generating energy, and more likely to respond to damage with inflammatory chemicals. To help find new ways to slow that decline, researchers in the laboratory of Rolf Bodmer, PhD, professor and director of the Development, Aging and Regeneration Program at Sanford Burnham Prebys Medical Discovery Institute (SBP), are looking at how the heart ages at a molecular level.

Bodmer’s team recently discovered a new potential contributor to cardiac aging, a protein called Odd, opening up a novel direction for research on therapies to prolong heart health. In their study, published in the journal Aging Cell, the gene for Odd, which controls the activity of other genes by turning them on or off, was found to be turned up in the hearts of old fruit flies. Bodmer’s lab studies flies because their hearts deteriorate with age in the same ways that human hearts do, but their genetics are much simpler.

“It’s intriguing that Odd is linked to aging because its known function is in early development—it’s crucial for the heart to form properly, and, as we found here, is also important for preventing the heart from deteriorating prematurely,” says Bodmer.

Odd’s involvement in cardiac aging was uncovered by a genome-wide comparison of the genes that are active in the hearts of young and old flies. Odd was one of over 200 genes whose activity was significantly elevated in older flies. Remarkably, further analysis showed that in aging hearts, increasing Odd activity temporarily protects the heart from decline by supporting proper electrical function and heart rate.

“Our findings suggest that increased levels of Odd in older hearts may be a way to compensate for aging-associated loss of function,” comments Bodmer. “In combination with a companion paper showing that another gene-regulating protein, FoxO, helps preserve the adult heart, they support a growing body of evidence that genes that are crucial in development are also important to keep the heart running well into old age.”

Bodmer contributed to the other paper, from the lab of Anthony Cammarato, PhD, assistant professor at Johns Hopkins University School of Medicine, and previously a staff scientist in Bodmer’s lab. The paper showed that FoxO helps protect the aging heart by turning on genes that help get rid of unneeded proteins.

“Following up on the findings of both studies could point to ways to keep our hearts working better for longer,” Bodmer adds.

The Bodmer lab paper is available online here and the Cammarato lab paper is here.

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Siobhan Malany, PhD, selected to conduct novel medical research in space

AuthorDeborah Robison
Date

June 13, 2016

ISS from space

Siobhan Malany, PhD, director of Translational Biology at Sanford Burnham Prebys Medical Discovery Institute at Lake Nona (SBP) and founder of the Institute’s first spin-off company, Micro-gRx, Inc., has been awarded $435,000 to study atrophy in muscle cells in microgravity on the International Space Station (ISS). In microgravity, conditions accelerate changes in cell growth similar to what occurs in the aging and disease process of tissues. Using real-time analysis, Malany will be able to rapidly study cells for potential new therapeutic approaches to muscle degeneration associated with aging, injury or illness. Continue reading “Siobhan Malany, PhD, selected to conduct novel medical research in space”

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Molecular “brake” prevents excessive inflammation

AuthorGuest Blogger
Date

February 25, 2016

Header image

Inflammation is a catch-22: the body needs it to eliminate invasive organisms and foreign irritants, but excessive inflammation can harm healthy cells, contributing to aging and sometimes leading to organ failure and death. A study published in Cell, co-authored by Jorge Moscat, PhD, and Maria Diaz-Meco, PhD, professors in SBP’s NCI-designated Cancer Center, in collaboration with the laboratory of Michael Karin, PhD, at the University of California, San Diego School of Medicine, shows that a protein known as p62 acts as a molecular brake to keep inflammation in check and avoid collateral damage. Continue reading “Molecular “brake” prevents excessive inflammation”

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Fine-tuning cellular energy increases longevity

AuthorJessica Moore
Date

February 25, 2016

Malene Hansen, PhD

New research from SBP has identified a protein that can extend the natural lifespan of C. elegans, a microscopic roundworm commonly used for research on aging and longevity. The findings, published in Cell Reports, expand what we know about the aging process and may lead to new ways to delay the onset of human age-related diseases such as cancer and neurodegenerative diseases. Continue reading “Fine-tuning cellular energy increases longevity”

Institute News

SBP’s 37th Annual Symposium: Aging and Regeneration

Authorsgammon
Date

November 3, 2015

Header image

On Friday, October 30, more 350 people came to SBP’s 37th Annual Symposium to hear leading scientists present their latest research on aging and regeneration.  The presenters, listed here, provided valuable insight into the latest studies on what causes aging, and strategies to repair injuries, prolong life, and prevent diseases.  The event was hosted by (from left to right): Rolf Bodmer, PhD, Malene Hansen, PhD, (in bee costume for Halloween) Alexey Terskikh, PhD

 

organizers-symposium-beaker

Many congratulations to Esther Minotti for successfully organizing the event!

symposium-photo-beaker

And many thanks to the Glenn Foundation for Medical Research for their support.