#112 - Ned David, Ph.D.: How cellular senescence influences aging, and what we can do about it

Jun 1, 2020 Episode Page ↗
Overview

Ned David, co-founder of Unity Biotechnology, explains cellular senescence and its impact on aging and age-related diseases. He discusses the development of senolytic medicines to treat conditions like osteoarthritis and macular degeneration, alongside entrepreneurial lessons.

At a Glance
10 Insights
2h 15m Duration
17 Topics
6 Concepts

Deep Dive Analysis

Defining Longevity and the Indignities of Aging

Three Principles of Aging: Malleability, Control Knobs, and Turnability

Evolutionary Examples of Disparate Lifespans

Control Knobs of Aging: IGF-1 Pathway and Caloric Restriction

Other Control Knobs: Young Blood, Mitochondrial Dysfunction, and Methylation Clock

Introduction to Cellular Senescence as a Druggable Mechanism

The Senescence Paradox: Anti-Cancer Role vs. Aging Driver

Historical Context of Cellular Senescence Discovery

The Senescence-Associated Secretory Phenotype (SASP) and its Harmful Effects

The Dual Role of SASP: Harmful in Aging, Beneficial in Wound Healing

Ned David's Journey to Focusing on Senescence and Unity Biotechnology

Risk Analysis Framework for Biotech Company Creation

Identifying Senolytic Molecules and Targeting Senescent Cells

Senolytics for Osteoarthritis: Animal Models and Human Clinical Data

Senescence in Atherosclerosis and Cancer

Future Applications of Senolytics: Macular Degeneration and Brain Health

Lessons from Kythera and Advice for Aspiring Scientists/Entrepreneurs

Cellular Senescence

A state where cells, after encountering unresolved stress, stop dividing permanently. These cells accumulate with age and contribute to various age-related diseases by secreting harmful factors, but also play a vital role in preventing cancer in younger organisms.

Senescence-Associated Secretory Phenotype (SASP)

A collection of over a hundred factors secreted by senescent cells into their microenvironment. These factors distort tissue function, driving inflammation and fibrosis, and contribute to the pathophysiology of aging and age-related diseases.

mTOR Complex

A master decision-maker biochemical system that regulates cell growth, division, and survival. It is influenced by nutrient availability (like in caloric restriction) and can be modulated by drugs like rapamycin to impact the rate of aging across species.

Methylation Clock

An ever-ticking clock based on the attachment or detachment of methyl groups to DNA over time. While its exact role is debated, changes in this epigenetic clock are correlated with aging and may contribute to noisy gene expression.

Yamanaka Factors

A set of four specific transcription factors that, when expressed in cells, can reprogram them into an embryonic-like state. This process can reset the methylation clock and induce features of youth in cells, though its application in whole organisms is complex.

Senolytic Molecules

Drugs designed to selectively target and eliminate senescent cells from the body. Unlike drugs that suppress cell secretions, senolytics aim to remove the source of harmful factors, potentially offering a more durable therapeutic effect with less frequent dosing.

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How does Ned David define longevity?

Ned defines longevity as the ability to live without the indignities of aging, such as profound degenerative disc disease or Alzheimer's, by using science and biology to change how we experience life.

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What are the three core principles of aging biology?

Aging is flexible and malleable, nature uses biochemical 'control knobs' to adjust lifespan, and these control knobs are now identifiable and turnable by scientists.

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How do cells decide between apoptosis and senescence when damaged?

Cells with DNA damage can either undergo programmed cell death (apoptosis) or enter a senescent state, but the specific factors that sway this decision are not yet fully understood.

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How do senescent cells, despite being few in number, cause widespread damage?

Senescent cells exert their harmful effects by secreting a variety of pro-inflammatory and pro-fibrotic factors, collectively known as the SASP, which distort the function of surrounding healthy tissues.

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Why did Unity Biotechnology focus on eliminating senescent cells rather than suppressing their secretions?

The decision was based on the potential for senolytic molecules to be dosed infrequently (e.g., once a year) because they remove the source of the problem, leading to a potentially safer and more effective drug compared to continuous suppression of secretions.

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What is the role of cellular senescence in cancer?

While the ability to make senescent cells is an important anti-cancer mechanism in young organisms, in older individuals, senescent cells in the tissue microenvironment may paradoxically become pro-cancer, delaying tumor formation but not necessarily preventing it.

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How does Ned David approach de-risking a bold idea in biotechnology?

He focuses on picturing the simple, beautiful end-state of the idea, then identifying the fundamental existential risks to that vision, and systematically building work plans and budgets to address each of those risks.

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What advice does Ned David offer to scientists considering an entrepreneurial path?

He advises against creating a false choice between academia and entrepreneurship, encourages animating one's work with a single beautiful idea that truly excites them, and stresses the importance of learning from more experienced and patient mentors.

1. Identify Existential Project Risks

When pursuing a bold idea, picture the desired end state and identify the fundamental, existential risks to that vision. This allows for focused effort and resource allocation.

2. Streamline Project Risks (2-4)

For any project, distill potential failure points down to 2-4 primitive, durable risks to maintain focus and simplify complex decision-making over many years.

3. Budget Aligned with Risks

Budget and build work plans that systematically address and remove each identified risk, ensuring efficient use of time and money.

4. Implement Go/No-Go Decisions

In academic or project settings, explicitly define failure modes and set clear criteria for go/no-go decisions after a set period to conserve time and pivot to more promising endeavors.

5. Adopt Project Portfolio Approach

Manage multiple projects simultaneously, understanding that it’s acceptable for some to fail, as long as at least one demonstrates success and warrants continued focus.

6. Avoid False Career Choices

Do not perceive academia and entrepreneurship as mutually exclusive paths; many successful individuals blend both, so take time to consider all options without rushing.

7. Animate Work with Beautiful Idea

Pursue a ‘single beautiful idea’ that genuinely excites you and gives you goosebumps, as this passion fuels perseverance through challenges.

8. Learn from Experienced Mentors

Actively learn from people who are more skilled and experienced and who are patient enough to teach, as this is crucial for developing necessary intellectual and emotional toolkits.

9. Preserve Senescent Cell Creation

Do not genetically or otherwise interfere with the body’s natural ability to create senescent cells, especially when young, as this system is vital for preventing tumor formation.

10. Favor Source-Eliminating Therapies

When considering future health interventions, prioritize those that eliminate the source of a problem (e.g., senescent cells) rather than merely suppressing symptoms, as this may lead to less frequent dosing and potentially safer outcomes.

Aging is not a rigid thing. So it's this flexible, malleable thing. And nature has throughout evolutionary history sort of bent and twisted aging for its own purposes to create creatures that have very different lifespans.

Ned David

The notion that you could essentially break the function of something or at least make it function a lot less well and double the lifespan of a creature was just a total mind warp for me and other people.

Ned David

If you want to know what the real biology is, it's the stuff that works in every lab, no matter who's doing it.

Ned David

The superpower of kids is the ability to make them, which prevents the replication of a cell that shouldn't replicate. And then it has the good sense to get rid of it before it harms anyone.

Ned David

The fact that eliminating these cells can produce a series of youth effects while not increasing cancer risk was very awesome and was actually kind of a theoretical validation of the picture in our minds about how this was all working.

Ned David

What motivated us was this would be a drug you would have to take all the time. And what we thought was so neat about the idea of making a molecule that could eliminate senescent cells, which we then named, we called them senolytic molecules. If you could make a senolytic molecule, you could dose it once.

Ned David

Cancer cells can divide and mutate and become anything to avoid death. They live under selective pressure, particularly in the context of drug. Senescent cells can't divide by definition. So their ability to access variation is dramatically reduced.

Ned David

De-risking a Bold Idea in Biotech

Ned David
  1. Picture the simple, beautiful end-state of the idea.
  2. Identify and write down the existential risks to that vision in the most primitive way possible (aim for 2-4 durable risks).
  3. Build work plans that systematically address and remove each identified risk.
  4. Develop budgets aligned with the work plans for risk removal.
  5. Politely seek funding from investors who understand and support the long-term vision.

Deciding Between Academic and Entrepreneurial Paths for Scientists

Ned David
  1. Avoid creating a false choice; recognize that both paths can involve company creation and offer unique freedoms/responsibilities.
  2. Animate your work with a single, beautiful idea that genuinely moves you and gives you goosebumps.
  3. Actively seek to learn from people who are more experienced, skilled, and patient than you, allowing them to teach you.
40 years
Lifespan of a hard clam If not eaten at a clam bake.
At least 500 years
Lifespan of a quahog (deep ocean clam relative) Compared to hard clam, a 12-fold difference.
Less than a year
Lifespan of a tiny shrew (shortest-living mammal) Compared to bowhead whale, a 200-fold difference.
At least 200 years
Lifespan of a bowhead whale (longest-living mammal) Estimate, as no one knows actual maximum.
2 to 3 years
Lifespan of a field mouse Compared to naked mole rat.
30 years
Lifespan of a naked mole rat 10 times longer than a field mouse.
Up to 50 times
Maximum cell divisions for human cells Before cells pull an emergency brake and stop dividing (senescence).
1% or less
Typical percentage of senescent cells in tissues Higher in some disease states.
About 30% longer
Lifespan extension in mice with senescent cell elimination When cells are eliminated from midlife until death.
100 to 1000 fold faster
Mitochondrial DNA mutation rate compared to nuclear DNA Leads to significant mitochondrial dysfunction with age.
5 years
Years for Darren Baker and Jan van dersen to publish paper on natural aging and senescence After 2011 paper, demonstrating senescent cells contribute to natural aging.
First most prevalent disease of aging
Prevalence of Type 2 Diabetes Osteoarthritis is the second most prevalent.
41%
Improvement in intervertebral disc volume maintenance in mice Observed when senescent cells were eliminated from midlife until death.
1 in 8
Proportion of age-associated macular degeneration patients with wet disease Treatable with anti-VEGF antibodies.
7 out of 8
Proportion of age-associated macular degeneration patients with dry disease Currently untreatable, but senolytics may play a role.
6.2
Average pain score (0-10 scale) for osteoarthritis patients at study entry At the highest dose of senolytic drug in Phase 1 study.
Just over 1
Average pain score (0-10 scale) for osteoarthritis patients at highest dose of senolytic Achieved within two weeks of injection and sustained for three months.