EoY 2022-AmyloSENS

AmyloSENS

Removing Junk from Between Cells

2022 End of Year Campaign

Week SEVEN

Challenging Heart Disease

No Damage Left Unchallenged!​

SRF AmyloSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why AmyloSENS:

To carry out their role in the biochemistry of our lives, the short-lived functional proteins produced by our cells need the flexibility to adopt several conformations over the course of their existence. But that flexibility comes with a risk. Every now and then, such a protein gets warped out of shape, and can adopt a malicious new shape that nullifies its essential purpose and makes it stick to other proteins of the same sort. These chains of mangled proteins then cause harm to our cells and tissues, either by being directly toxic to cells or by forming deposits in our tissues that physically interfere with their mechanical function. As we age, these “amyloid” proteins accumulate in our tissues and eventually cause them enough problems that they can’t carry out their purpose. The symptoms caused by that tissue dysfunction are what gets diagnosed as a disease of aging, and includes some of biological aging’s most fearsome cripplers and killers. With antibodies and other biotechnologies, these amyloids can be removed from our tissues, freeing them to function again. Support AmyloSENS, and clear our tissues of the rubble!

AmyloSENS: Ask Me Anything:

With Dr. Sudhir Paul & Michael Rae

This week's Life Noggin video:

Disease Focus: Heart Disease

When people say “heart disease,” they most often mean atherosclerosis — which is not actually a disease of the heart itself, but of the blood vessels. A much more literal form of heart disease is caused by amyloids that deposit in the aging heart. These amyloids are chains of malformed units of the transport protein transthyretin (TTR) or several other proteins, which twist out of shape, bind together in chains, and infiltrate into the gaps between the heart muscle cells. These deposits then physically get in the way of the heart muscle’s attempts to expand and contract as it needs to do to keep the precious blood of life flowing to our tissues. They also often interfere with the nerves that control the heart’s beating, causing it to spasm at the wrong time. People suffering from heart failure get short of breath when they exercise, with the limits of their endurance slowly closing tighter and tighter around them; their ankles swell, followed by their livers and other parts of the body; their hearts may beat too quickly or with episodes of dangerous erratic beats. Eventually, they die when their heart simply can’t do its job well enough, or because a clot forms in the blood that pools in the failing heart’s chambers and triggers a stroke or a pulmonary embolism. Support AmyloSENS so all our hearts can beat strong!

Watch the AmyloSENS approach animation:

To learn more about AmyloSENS

Show your support for

AmyloSENS

Stay tuned next week for our campaign finale!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022-OncoSENS

OncoSENS

Making Cancerous Mutations Harmless

2022 End of Year Campaign

Week SIX

Challenging Cancer

No Damage Left Unchallenged!​

SRF OncoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why OncoSENS:

The genes in the nucleus of our cells have long been described as the “book of life,” but perhaps “the cookbook of life” would be more precise. Our genetic code contains the instructions your cells use to produce all the signaling factors, microscopic machines, and barriers that comprise our bodies and keep us alive and healthy. So you can imagine what can happen to a cell when a censor tears pages out of that book or crosses out offending words, or when a vandal scrawls text midsentence at the page break to transform a line into gutter humor. That’s what mutations (and epimutations) are: they delete or distort the instructions our cells need to make the stuff of life.

Because each mutation happens to a single cell in isolation, many mutations are harmless, because they hit a gene for some protein that the cell type where they occur doesn’t use — like the gene for a liver enzyme in a lung air sac cell. Others are mild and barely affect function. And even when a mutation severely interferes with a cell’s ability to do something important, the effect is often limited simply because it is limited to one cell out of millions or billions in a tissue that can pick up the slack.

But there are particular kinds of mutations that really can ruin a life. Fixing these mutations is impossible with the biotechnology of today and our near tomorrow — but we can prevent them from doing harm by going one link higher up in the chain and preventing the mutant cells themselves from doing harm. Support OncoSENS, and defang the mutant horde!

A SENS Conversation

With Dr. Ravi Jain & Michael Rae

This week's Life Noggin video:

Disease Focus: Cancer

Cardiovascular diseases are the number one killer in most wealthy countries — but cancer is a very close second, and it’s a disease that still strikes much more fear. In part, that’s because we don’t yet have the equivalent of statins and blood pressure drugs for holding off cancer, and in part because despite decades of work, treatment for many cancers is still a terrible ordeal with not great outcomes.

What makes cancer such a fearsome opponent is that it harnesses the power of evolution. Every treatment you throw at a tumor acts as a selective pressure in a population of hundreds of billions to trillions of cells that replicate and mutate at a ferocious pace. And it only takes a single cancer cell with a mutation that lets it escape a given therapy for the cancer to regroup and grow back.

The root of cancer is mutations, but what makes them deadly is the effects of those mutations: out-of-control growth. If we can irreversibly disable cancer cells’ ability to replicate themselves, mutation-bearing cells could be defanged. They would grow large enough to form benign little lumps in our bodies and then come to a sputtering halt. These benign growths could then be safely and permanently plucked out by a surgeon. Support OncoSENS, and run cancer out of gas!

Watch the OncoSENS approach animation:

To learn more about OncoSENS

Show your support for

OncoSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022RepleniSENS

RepleniSENS

Replacing Lost Cells

2022 End of Year Campaign

Week FIVE

Challenging Parkinson's

No Damage Left Unchallenged!​

SRF LysoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why RepleniSENS:

Life begins with the cell, and ultimately it ends with them. Throughout our lives, we’re losing cells for one reason or another. Some cells are destroyed by trauma or being cut off from their blood supply. Some are designed to slough off, like outer skin cells and cells on the surfaces of our GI tract. And some self-destruct after they’ve served their purpose or if they sense themselves to be in danger of becoming cancerous. For many of these cells this is no big deal: they’re more or less interchangeable and the body easily replaces them. But others are hard to replace — or they become hard to replace due to aging changes in the organ. Meanwhile, the stem cells that are supposed to replace them can themselves become depleted due to aging processes. And there are a few critical cells (like most brain neurons and heart muscle cells) that don’t get replaced at all: they’re designed to last a lifetime, but not the kind of lifetime we live today or want to live in the future. Support RepleniSENS, and bring back what you’ve been missing!

RepleniSENS: Ask Me Anything:

With Dr. Abdlelhadi Rebbaa & Michael Rae

With Dr. Jean Hébert & Michael Rae

This week's Life Noggin video:

Disease Focus: Parkinson's

The most recognizable signs of Parkinson’s disease — the hand tremors, the stony face, the loss of balance — are the result of the loss of a specific kind of nerve cell in a specific region of the brain. These neurons are responsible for producing the brain messenger-molecule dopamine and delivering it in a precisely controlled way to a region of the brain involved in motion control. As we age, all of us gradually lose these cells, and some people lose them more quickly because of genetics or lifestyle and environmental factors. When our reserve of these cells falls below a critical threshold, the remaining cells can no longer properly guide the motion center. Our fine control of our motion degrades, and our hands begin to tremble. The symptoms worsen over time as more neurons are lost, and the drugs used to control symptoms become less and less effective and harder and harder to manage.

Scientists have worked for decades on RepleniSENS therapies for people suffering with Parkinson’s, and it’s been a learning process: some patients in these trials have benefitted hardly at all, but others have had remarkable recoveries that free them from drugs for years. They are now working on new trials, using the powerful new biotechnology of cellular reprogramming  create custom cells of just the right kind, and using new surgical techniques to deliver them to just the right place. Support RepleniSENS so we’ll all move freely again!

Watch the RepleniSENS approach animation:

To learn more about RepleniSENS

Show your support for

RepleniSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022-GlycoSENS

GlycoSENS

Repairing the Extracellular Matrix

2022 End of Year Campaign

Week FOUR

Challenging Stroke

No Damage Left Unchallenged!​

SRF GlycoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why GlycoSENS:

When we think about what makes us tick, we think about cells. But those cells would be nothing more than human pond scum spread out over the earth’s surfaces if they weren’t shaped, supported, and in signaling networks with the meshwork of biological proteins known as the extracellular matrix, or ECM. The ECM shapes the heart’s four chambers and the familiar outlines of our kidneys and livers. And it’s the flexible, functional tubing that carries blood from the pumping heart out to the lungs to gather life-giving oxygen, and then back to the heart, where yet more ECM proteins distribute oxygen and nutrients to our brains, muscles, and inner organs — even the heart itself. But the ECM becomes damaged with aging, stiffening our hearts so they can’t pump effectively, and making our arteries less flexible. The loss of elasticity in our arteries causes our blood pressure to rise, and robs them of their ability to buffer the delicate structures of our kidneys and brains against the pounding pulse.

The ECM is the scaffold and support that binds our bodies together and sculpts and signals how our cells behave. Like the frame of a house, when it breaks down, everything else falls down with it. Hold it together: support GlycoSENS!

GlycoSENS: Ask Me Anything:

With Dr. Jonathan Clark & Michael Rae

This week's Life Noggin video:

Disease Focus: Stroke

Stroke is the number three killer worldwide, responsible for the deaths of over six million people a year. And that’s only the beginning of the misery it causes: survivors can suffer changes in their emotions and personalities, and lose the ability to walk; to see; to control their bladders; to express their feelings and thoughts in speech. And even if controlled, their muscles can become weak, and their hands or feet are too numb for everyday use. Damage to the nerves controlling yet other organs can also leave survivors more vulnerable to pneumonia and pressure sores.

Like all diseases of aging, there is no one cause of stroke. But the most important factor that accelerates vulnerability to strokes and acutely triggers them is the age-related rise in blood pressure — and that, and the stiffening of the arteries, is substantially down to damage to the arterial ECM. Support GlycoSENS, and restore the brain’s protective buffer!

Watch the GlycoSENS approach animation:

To learn more about GlycoSENS

Show your support for

GlycoSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022-LysoSENS

LysoSENS

Clearing Waste Accumulations Out of Cells

2022 End of Year Campaign

Week THREE

Challenging Atherosclerosis

No Damage Left Unchallenged!​

SRF LysoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why LysoSENS:

How much do you enjoy a sanitation strike — or (dare we say it) a clogged toilet? Now think about that happening in your cells! The lysosome is the cell’s recycling center. It takes cellular components that are damaged or past their prime, breaks them down into useful raw materials, and returns them to the cell to build shiny new cell-stuff. But now and again something gets into the lysosome that it just can’t break down, and instead just sits there. Over time, more and more of these stubborn wastes get stuck in the lysosome, until they reach the point that —like the monstrous London “fatberg” — they back the whole system up disastrously, paralyzing the cell. Without a functioning lysosome, our aging cells become increasingly dysfunctional, and disease and debility stalk close behind.

The main LysoSENS strategy is for scientists to cook up Drāno® for our cells: powerful enzymes that can break down the stubborn wastes that clog up our lysosomes. With the clog broken down, the lysosome can “flush clear” again and restore normal function to the cell. Keep it clean: support LysoSENS!

LysoSENS: Ask Me Anything:

With Dr. Matthew O'Connor & Michael Rae

This week's Life Noggin video:

Disease Focus: Atherosclerosis

Cardiovascular disease is the number one killer worldwide, and atherosclerosis — the cholesterol-laden deposits inside our artery walls — is the lion’s share of cardiovascular diseases. Atherosclerosis begins when the particles that carry cholesterol amongst our cells occasionally get stuck in the artery wall, and the body sends in a sanitation worker called a macrophage to remove it. Initially this works fine, but damaged forms of cholesterol cause problems for the macrophage’s lysosome, and eventually it becomes poisoned and disabled, stuck in the artery wall and sending out signals to attract more macrophages to help it. But this just makes the situation worse! The buildup of these dysfunctional macrophages is the fundamental basis of atherosclerotic plaque, which increasingly disrupts the artery wall until it eventually bursts, triggering a blood clot that speeds down the blood vessels to the heart or the brain, triggering heart attacks and strokes.

By equipping our cells with enzymes that can break down the damaged cholesterol products in their lysosomes, we can restore the macrophages to health, allowing them to pack up and leave the artery wall — much like a patient leaving the hospital after an infection has finally cleared. With the dysfunctional macrophages finally out of the way, the inflammation at the site cools off, and the lesion in the artery can heal itself. Support LysoSENS, and help prevent and cure atherosclerosis and other diseases of clogged-up cells!

Watch the LysoSENS approach animation:

To learn more about LysoSENS

Show your support for

LysoSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022-MitoSENS

MitoSENS

Preventing Damage from Mitochondrial Mutations

2022 End of Year Campaign

Week TWO

Challenging Sarcopenia

No Damage Left Unchallenged!​

SRF MitoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why MitoSENS:

The mitochondria are the powerhouses of the cell! What else do you need to know? All the processes in every cell in the body that keep you alive and able to do anything at all depend on cellular energy, and the mitochondria are where that energy gets made. But like other kinds of power plants, mitochondria produce toxic wastes along with valuable power. And that cellular pollution can damage the genes that mitochondria need to produce the replacement parts that keep their energy-production lines running. When these genes are damaged badly enough, the cell can’t produce energy efficiently, and the cell is forced to adopt an abnormal metabolic state that hobbles its normal function and harms its neighbors.

The core MitoSENS strategy is to bypass these mutations by creating “backup copies” of the mitochondrially-encoded genes in the safe harbor of the nucleus. That way our mitochondria can always get the spare parts they need, allowing them to keep fueling us into an indefinite healthy life.

MitoSENS: Ask Me Anything:

With Dr. Amutha Boominathan & Michael Rae

This week's Life Noggin video:

Disease Focus: Sarcopenia

If you compare two people of different ages with the same amount of muscle, the older person will still be weaker than the younger person. Even lifelong athletes who train regularly and get plenty of protein still suffer both a loss of muscle mass with age and a disproportionate and precipitous loss of strength on top of that. It’s called sarcopenia, and it’s a major contributor to frailty and loss of independence with age. When you see an older person struggling to open a door or open a jar of food, or who needs help getting luggage into the overhead compartment in an airplane, that’s sarcopenia at its terrible work. Sarcopenia also impacts our lives in less obvious ways, like increasing our risk of falling and of suffering a disabling fracture if we do. It even contributes to aging people’s increased risk of developing and dying from pneumonia, as weakened diaphragm muscles make it harder to fill our lungs with precious air and to cough out mucus or food and drink caught in the airways.

What’s that got to do with MitoSENS? Large deletions in mitochondrial DNA are an important and underappreciated driver of sarcopenia. Muscle fibers are organized into segments, each with its own localized population of mitochondria. When one of these local populations is overtaken by these defective mitochondria, that segment becomes the weak link in the chain of the muscle fiber. Such defective segments deplete the muscle’s ability to generate force and can even be the site of a break, taking the entire muscle fiber out of service. Fund MitoSENS, and help keep our muscles working and our fires burning bright!

Watch the MitoSENS approach animation:

To learn more about MitoSENS

Show your support for

MitoSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

EoY 2022-ApoptoSENS

ApoptoSENS

Removing Dysfunctional Cells

2022 End of Year Campaign

Week ONE

Challenging Alzheimer's

No Damage Left Unchallenged!​

SRF ApoptoSENS NFTs!

Example of a sample data feed that will constitute the NFT:

In collaboration with digital artist

*If you are donating via cryptocurrency or NFT and would like to vote on which strand should receive a RFP for 2023, please send us an email address we can associate with your donation so that we can issue voting tokens to you.

Earn SENS tokens for every donation…

…then use your tokens to vote – and the strand with the most support will receive a new RFP (Request for Proposals) for 2023!

Why ApoptoSENS:

It’s bad enough that we lose cells with age. Adding insult to injury, our remaining cells can go rogue and start attacking or interfering with the healthy cells around them. These senescent cells throw a kind of cellular emergency brake on themselves when they suffer damage. Like some cars after a crash, their car alarm (in this case, inflammatory and other immune signals) goes off and won’t stop, which drives the whole neighborhood crazy! In the presence of blaring signaling from such abnormal cells, normal cells can’t do their job, which robs us of our health as our tissues become increasingly dysfunctional.

It’s these and other rogue cells that ApoptoSENS targets for termination — with extreme prejudice! We already have seen from animal models that destroying abnormal cells causes a dramatic rejuvenation of old mice and can prevent and even reverse diseases of aging. Support ApoptoSENS so we can do the same for aging humans!

ApoptoSENS: Ask Me Anything:

With Dr. Amit Sharma & Michael Rae

This week's Life Noggin video:

Disease Focus: Alzheimer's

Of all the misery that degenerative aging inflicts on us, it’s the loss of our memories and identity in Alzheimer’s and other dementias of aging that most people fear most. Too many of us have already watched helplessly as our parents and grandparents or a friendly older neighbor have slowly lost touch with themselves, forgotten who we are, and slipped into helpless confusion and death. In animal models, destroying senescent cells in the brain can greatly postpone and ameliorate the course of genetic models of Alzheimer’s. Support ApoptoSENS and speed the day we may be able to do the same for our loved ones!

Watch the ApoptoSENS approach animation:

To learn more about ApoptoSENS

Show your support for

ApoptoSENS

Stay tuned next week for more of the 7 Strands approach!

AmyloSENS ApoptoSENS GlycoSENS LysoSENS MitoSENS OncoSENS RepleniSENS

Media Partner:

Ending Aging Forum 2022

Ending Aging Forum 2022

Research & Education

September 2nd - 3rd, 9am – 2:30pm PST

EXVO Virtual Reality Platform

Thank you for a wonderful and thought provoking time with the team at SENS Research Foundation. This virtual event allowed us to share first-hand, the latest advances that our in-house researchers are making toward new rejuvenation biotechnologies, along with some of our young scientists-in-training and outside researchers whose research we fund. In addition to the formal presentations, we enjoyed the opportunity to facilitate one-on-one discussions with the scientists and other members of our team, as well as with citizens, donors, and activists who dream of and work for a future free of degenerative aging.

Breaking down the barriers to attendance, we hosted the virtually through EXVO, a strong platform for this VR experience. The virtual event’s presentations were made in our Conference Hall, along with project-specific Research Booths and booths for scientific posters presented by our students that broke down different research projects.

In the Expo Room, attendees were also able to meet and talk one-on-one or in small groups with the team and other supporters, or watch videos in which our team members and scientists-in-training introduce themselves and what drew them to this Mission.

Stay tuned for upcoming YouTube videos of the presentations to learn and celebrate how far we’ve come, and to catch a glimpse of the future we’re building!

Intramural Speakers

Dr. Amit Sharma

Dr. Amit Sharma

Group Lead, Senescence Immunology Research

Amit received his PhD from the University of Pune for demonstrating microRNA regulation of cytokines and regulation of allergic inflammation. During his postdoctoral research at Stanford University, he demonstrated age-related resistance in the reprogramming of fibroblasts with classical Yamanaka factors. To peruse his interest in aging, he did a second postdoc at the Buck Institute in investigating molecular regulatory pathways involved in genotoxic stress and cellular senescence in invertebrate and mammalian models. He joined SENS Research Foundation as Group Lead in 2019 and his laboratory focuses on developing strategies to harness the immune system in mitigating the deleterious effects of senescent cells.

Dr. Tesfahun Admasu

Research Fellow​

Dr. Admasu earned his PhD in Biochemistry from national university of Singapore. In his PhD work he investigated interactions between lifespan extending drugs with the aim of engineering synergistic benefits in C. elegans. Dr. Admasu is currently a research fellow at SENS Research Foundation. His research focus on isolation and characterization of secondary senescent cells using surface markers and identification of novel approaches to ablate multiple types of senescent cells. He recently identified a novel senolytic approach to kill multiple types of senescent cells.

Dr. Amutha Boominathan

Group Lead, MitoSENS

Dr. Amutha Boominathan is the Group Lead for the MitoSENS program at SENS Research Foundation. She joined the organization in 2013 as a Senior Research Scientist and became the Group Lead for the program in 2016. She has a PhD in Biochemistry and has over 22 years of experience in mitochondria biology.

Dr. Abdelhadi Rebbaa

Group Lead, RepleniSENS

Dr. Rebbaa received his PhD from Claude Bernard University, Lyon, France, and held research and faculty positions at Northwestern University, the University of Pittsburgh and Columbia University.  Over the course of his career, his research encompassed target and drug discovery and development in the fields of cancer, stem cells and aging. Recently, he oversaw the discovery and preclinical testing of small molecule senolytics and biomarkers of aging.

Dr. Rebbaa served as a Principal Investigator on multiple grants, published over 40 manuscripts and reviewed manuscripts in respected scientific journals. He is currently applying the acquired experience to study the effect of a combination therapy using senolytics and stem cell transplantation on reducing senescent cell burden and the functional decline caused by aging.

Extramural Speakers

Dr. Tilman Grune

Scientific Director, German Institute of Human Nutrition Potsdam-Rehbruecke (DiFE)

Dr. Grune trained as a biochemist in Moscow. Later he obtained his PhD and D.Sci. at the Charité Berlin. After Post-Doc positions in Berlin and Albany; NY he is heading its own laboratory in Berlin and Düsseldorf. After professorships in Stuttgart and Jena, he is now the Scientific Director of the German Institute of Human Nutrition and the head of the Department of Toxicology. Since 2020 he holds also a position of a professor of Physiological Chemistry and Cellular Biochemistry at the University of Vienna, Austria. His scientific interest is focused on the aging of post-mitotic cells, nutritional effects on aged cells and biomarkers of nutrition, aging and redox status. He is founding Co-Editor- in-Chief of Redox Biology and has published some 450 publications.

Dr. Jean Hebert

Professor, Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine

Jean trained as a molecular geneticist, obtaining his Ph.D. from the University of California, San Francisco, before specializing in the study of how neural stem cells form the brain at Stanford University. He is now a Professor at the Albert Einstein College of Medicine in New York.

Dr. Jonathan Clark

Head of Biological Chemistry Facility, Babraham Institute, Cambridge

Jonathan studied Biological Chemistry at the University of Leicester and then obtained a PhD in new synthetic methods towards the synthesis of Taxol. He then spent 11 years working in the biotechnology sector around Cambridge, UK before joining the Babraham Institute where he now runs the Biological Chemistry group. His group has been studying the ageing of collagen with the aim of understanding how chemical changes which occur in collagen with age impact function.

Dr. Andrei V. Gudkov

Garman Family Chair in Cell Stress Biology, Roswell Park Comprehensive Cancer Center

Dr. Gudkov obtained his Ph.D. and D.Sci. degrees in Moscow, USSR. Since 1990, works in the US: first, at University of Illinois at Chicago, then in Cleveland Clinic and, since 2007, at his current position of Sr.VP, Professor of Oncology and Chair of Department of Cell Stress Biology at Roswell Park Comprehensive Cancer Center in Buffalo, New York. His interests involve anti-cancer and anti-aging research, radiation biology, virology and mechanisms of inflammation. He published >250 papers, serves on editorial boards of Aging, Oncogene, Oncotarget (Co-Editor-in Chief), etc., and founded several biotech companies that develop anticancer and anti-aging drugs based on his inventions.

Students Presenting Posters

Oliver Frost

Ph.D. Student

Ashley Brauning

Masters Student

Marek Pinto

Summer Scholar

Keefer Li

Summer Scholar

Benjamin Ramsell

Summer Scholar

Mustafa Mahmood

Summer Scholar

Alec Eames

Summer Scholar

Sheryl Lin

Summer Scholar

Chinkuli Munkombwe

Summer Scholar

Nikita Sajeev

Summer Scholar

Grace Goetz

Summer Scholar

Rushmeen Tariq

Summer Scholar

Bronwyn Mogck

Summer Scholar

Anastasiia Rudenko

Summer Scholar

Schedule

September 2nd - 3rd, 9am – 2:30pm PST

(schedule subject to change prior to the event)

Posters prepared by graduates of our Education programs will be available to view throughout the event.

Friday Sept 2nd: Day 1

9am – 9:30am: Meet & Greet at Conference Hall / Booths Open

Student Booths Featured:
  • Marek Pinto
  • Keefer Li
  • Benjamin Ramsell
  • Mustafa Mahmood
  • Chinkuli Munkombwe
  • Nikita Sajeev

9:30am – 10:30am: ApoptoSENS

Dr. Amit Sharma – 1 hour (45 min talk plus 15 min Q+A)

10:30am – 11:30am: Dr. Tilman Grune

1 hour (45 min talk plus 15 min Q+A)

11:30am – Noon: 30-minute break

Student Booths featured:

  • Grace Goetz
  • Browyn Mogck
  • Rushmeen Tariq
  • Sheryl Lin
  • Oliver Frost
  • Ashley Brauning
  • Anastasiia Rudenko

Noon – 12:45pm: ApoptoSENS

Dr. Tesfahun Admasu: 45 min (30min talk plus 15 min Q+A)

12:45pm – 1:45pm: Dr. Jean Hebert

1 hour (45 min talk plus 15 min Q+A)

1:45pm – 2:30pm: Booths Open

End of Event Day 1

Sat Sept 3rd: Day 2

9am – 9:30am: Meet & Greet at Conference Hall / Booths Open

Student Booths Featured:
  • Grace Goetz
  • Browyn Mogck
  • Rushmeen Tariq
  • Sheryl Lin
  • Oliver Frost
  • Ashley Brauning
  • Anastasiia Rudenko

9:30am – 10:30am: MitoSENS

Dr. Amutha Boominathan – 1 hour (45 min talk plus 15 min Q+A)

10:30am – 11:15am: RepleniSENS

Dr. Abdelhadi Rebbaa 45 min (30min talk plus 15 min Q+A)

11:15am – 11:45am: 30-minute break

Student Booths featured:

  • Marek Pinto
  • Keefer Li
  • Benjamin Ramsell
  • Mustafa Mahmood
  • Alec Eames
  • Chinkuli Munkombwe
  • Nikita Sajeev

11:45am – 12:45pm: Dr. Jonathan Clark

1 hour (45 min talk plus 15 min Q+A)

12:45pm – 1:45pm: Dr. Andrei Gudkov

1 hour (45 min talk plus 15 min Q+A)

1:45pm – 2:30pm: Networking

End of Event Day 2

Intramural Speakers' Summaries

Dr. Amit Sharma

Eliminating senescence: more ways to kill death resistant cells from novel senolytics to immune based therapeutics.

Many aging pathologies are causally linked to the accumulation of senescent cell burden with increasing age. The senescent cells are characterized by molecular and structural changes culminating in an irreversible cell-cycle arrest and secretion of complex pro-inflammatory senescence-associated secretory phenotype (SASP), which contributes to chronic inflammation and damage to surrounding cells and tissues. Thus, the removal of senescent cells via drugs that selectively kill senescent cells (“senolytic” drugs) to prevent or delay tissue dysfunction has shown great promise in improving age-related pathologies and extending health span.

The research goals of my laboratory are to (A) investigate the cellular mechanisms that cause age-dependent increase in cellular senescence burden and (B) investigate interventions that reduce or eliminate senescent cells.

Several lines of evidence show that Natural Killer (NK) cells play a vital role in the immune surveillance of these cells. Despite these recent studies, therapeutic strategies to exploit NK cells to reduce the senescence burden have not yet emerged. We are investigating mechanisms involving NK cell-mediated targeting of senescent cells to improve NK cell-mediated senotherapeutics for the treatment of aging and inflammatory disorders.

Dr. Tesfahun Admasu

Dissecting primary and secondary senescence to enable novel senotherapeutic strategies.

Senescent cells can spread the senescent phenotype to other cells by secreting factors called the Senescence Associated Secretory Phenotype (SASP). The resulting secondary senescent cells make a significant contribution to the burden of senescent cells accumulation with age. Efforts made to characterize secondary senescence have mostly been unreliable due to their analysis based on mixed populations of senescent and non-senescent cells. Here, we used dipeptidyl peptidase-4 (DPP4) as a surface maker to isolate senescent cells from mixed populations. Using this novel technique, we enriched the percentage of secondary senescent cells from 40% to 85%, which is comparable to senescence induction levels in primary senescent cell cultures. We then used this enriched culture to dissect the molecular and phenotypic differences and similarities between DPP4+ isolated primary and secondary senescent cells. Notably, we found that secondary senescent cells have distinct prosurvival mechanisms and are substantially less susceptible to current senolytics than are primary senescent cells. Finally, we identified a novel and broad- spectrum senolytic approach to ablate both primary and secondary senescent cells.

Dr. Amutha Boominathan

Allotopic expression of mtDNA genes.

Mitochondrial dysfunction has been implicated in several age-related diseases and aging in general. Accumulation of mutations in the mtDNA with age adversely affects the organelle function and the MitoSENS group at SENS Research Foundation endeavors to identify translational avenues in maintaining the fitness of mitochondria over time using a gene therapy approach. Utilizing codon optimization to synchronize the nuclear and mitochondrial DNA genes, the team recently reported robust transient expression for all the 13 protein coding genes in the mitochondrial DNA. In patient derived cybrid cells and animal models with specific mutations the team was further able to demonstrate that allotopic gene expression for one of the two Complex V mitochondrial DNA genes, namely ATP8, restored several functions including protein expression, complex integration, and recovery of OxPHOS function. Efforts to achieve stable expression with functional relevance for the rest of the 12 genes are ongoing.

Dr. Abdelhadi Rebbaa

Combination of senolytics and stem cell transplantation as a potential anti-aging therapy

The accumulation of damaged/senescent cells in the body with time is a hallmark of aging. Since these cells produce pro-inflammatory and pro-fibrotic molecules, they are believed to contribute to the onset and/or the severity of the chronic diseases that accompany old age. Based on this, the development of strategies to eliminate senescent cells for instance by using senolytics has opened new possibilities for anti-aging therapeutic development. Prior to the discovery of senolytic agents, evidence was provided that local or systemic transplantation of mesenchymal stem cells improve the outcome of various aging associated diseases. Although the underlying mechanism of their action is still not well defined, it is believed to be mediated by paracrine and immunomodulatory effects.

Here we set out to test the hypothesis that the combination of senolytics with mesenchymal stem cell transplantation will have a synergistic effect in extending mouse health span. In vitro and in vivo studies are underway to identify adequate biomarkers and imaging techniques to monitor response to the anti-aging interventions to be tested. We are also conducting cell-based analyses to select a senolytic candidate and to assess the quality and suitability of the MSC cells to be used in in vivo. Finding from this study will allow for evaluating the efficacy of candidate senolytics in reducing senescent cell burden in mice and whether their combination with stem cells will enhance health span of the treated animals.

Extramural Speakers' Summaries

Dr. Tilman Grune

LIpofuscin – an active player in senescent cells and how to get rid of it

Lipofuscin is an aggregate of cross-linked, non-functional proteins and other cellular components accumulating mainly in post-mitotic cells. Many of other studies revealed that it is impairing cellular function and, therefore, contributes to the age-associated functional organ decline. Besides studying the effects of lipofuscin in post-mitotic cells we are in the process of developing strategies to reduce the lipofuscin burden.

Dr. Jean Hebert

Brain cell and tissue replacement as a cornerstone to beating aging.

The neocortex is the part of our brain that performs our highest cognitive functions. In recent years, the mechanisms underlying how stem cells in the embryo generate the neocortex have become better understood. Armed with this knowledge, the Hébert Lab is developing approaches to replace and repair adult neocortical tissue after age-related degeneration.

Dr. Jonathan Clark

A different perspective on the changes in tendon collagen crosslinking with age and the impact on function.

In his presentation Jonathan will discuss and interpret results from his group on the changes in tendon collagen crosslinking with age and the impact on function. In this work it is shown that statements often made about crosslinking and ageing are over simplifications and that the situation is actually more subtle and dynamic than previously recognised. This work suggests that if you are to rejuvenate tendon collagen, that you probably have to tackle the changes at multiple levels and not just remove irreversible crosslinks. Two publications from his group relevant to this presentation can be found at: https://pubmed.ncbi.nlm.nih.gov/32381510/ and https://pubmed.ncbi.nlm.nih.gov/32546479/

Dr. Andrei V. Gudkov

Endogenous “retrobiome” as a putative aging driver.

Nearly half of the human genome is occupied by retrotransposons, highly repetitive interspersed virus-like genetic elements that replicate via reverse transcription. This “retrobiome” is epigenetically repressed in normal cells but is frequently desilenced in cancer cells. In addition to tumors, retrobiome expansion also occurs in aging somatic cells contributing to aging-associated DNA damage and inflammation. Our team isfocused on developing mouse models that would enable testing the role of derepression of retroelements in aging and testing antiaging therapies targeting retrobiome activity.

Student Bios

Oliver Frost

Ph.D. Student from Loughbrough University, hosted by Abdelhadi Rebbaa at SENS Research Foundation

Oliver is a PhD student from the University of Loughborough, a top ten university in the UK. Based in the RepleniSENS team with Dr. Rebbaa, his project focuses on the synergistic effects of senolytics followed by a stem cell transfer to improve health and lifespan in mice.

Ashley Brauning

Masters Student from Dominican University of California, hosted by Amit Sharma at SENS Research Foundation

Ashley received her B.S in Molecular and Cellular Biology from the University of Puget Sound and is currently working on her M.S at Dominican University. She joined SRF in September 2021 as a post-baccalaureate research fellow and graduate student researcher with the ApoptoSENS group using surfaceomics techniques to characterize the surface of senescent cells.

Marek Pinto

Summer Scholar from Boston University, hosted by Amutha Boominathan at SRF

Marek Pinto is a rising sophomore at Boston University studying Biomedical Engineering and Computer Science. Marek is fascinated by the mechanisms behind aging and has been excited to contribute to research through the SRF program this summer!

Keefer Li

Summer Scholar from University of Massachusetts, Amherst, hosted by Amutha Boominthan at SRF

Keefer Li is a junior Biochemistry and Molecular Biology major in the Commonwealth Honors College at the University of Massachusetts Amherst. Keefer has been super excited to spend his summer living and learning with fellow anti-aging enthusiasts in Mountain View, California.

Benjamin Ramsell

Summer Scholar from Oregon State University, hosted by Abdelhadi Rebbaa at SRF

The mechanisms of aging is a field of research that Benjamin Ramsell has been fascinated with since he was twelve. At SRF, he feels that he has the opportunity to study these mechanisms directly and contribute to the development of medical science.

Mustafa Mahmood

Summer Scholar from Siena College, hosted by Abdelhadi Rebbaa at SRF

Mustafa Mahmood is a rising senior majoring in Biology. Mustafa is most excited about getting some hands-on experience in aging research and increasing the breadth of his research experience with the SRF program!

Alec Eames

Summer Scholar from University of Michigan Ann Arbor, hosted by Cyclarity

Alec Eames is a biomedical engineering student at the University of Michigan. Alec is looking forward to contributing to the cutting-edge aging research SRF is conducting in aging biology!

Sheryl Lin

Summer Scholar from Johns Hopkins University, hosted by Aspen Neurosciences

Sheryl Lin is a rising junior studying Molecular and Cellular Biology at Johns Hopkins. Sheryl is thrilled to be contributing to the fight against Parkinson’s Disease and working with cutting-edge autologous neuron replacement therapies at Aspen Neuroscience.

Chinkuli Munkombwe

Summer Scholar from Georgia State University, hosted by Evan Snyder at Sanford Burnham

Chichi Munkombwe is a neuroscience major at Georgia State University. As part of the SRF Summer Scholars Program, Chichi looks forward to learning new methods of tackling the questions in her field and collaborating with other members of her cohort!

Nikita Sajeev

Summer Scholar from Temple University, hosted by Evan Snyder at Sanford Burnham

Nikita Sajeev is currently a senior neuroscience major at Temple University in Philadelphia, though her hometown is Portland, Oregon. Nikita is interested in science communication and clinical care, and hopes to eventually be a physician scientist.

Grace Goetz

Summer Scholar from University of Connecticut, hosted by Evan Snyder at Sanford Burnham

Grace Goetz, is a rising senior at the University of Connecticut. Grace is a biomedical engineering major with a concentration in biomaterials and tissue engineering, and researcher with the Tissue Engineering Sciences and Technology lab on campus.

Rushmeen Tariq

Summer Scholar from University of Utah, hosted by Christopher Wiley at Tufts University

Rushmeen Tariq is a biology major at the University of Utah. Rushmeen has been really excited to do research and explore Boston this summer!

Bronwyn Mogck

Summer Scholar from Villanova University, hosted by Christopher Wiley at Tufts University

Bronwyn Mogck and is a junior at Villanova University double majoring in Biology and Humanities. Bronwyn is interested in looking at the way that lab research leads to changes in everyday lives, and admires the way SRF values communication with the non-scientific community.

Anastasiia Rudenko

Summer Scholar from Pace University, hosted by Jennifer Garrison/Polina Lishko at The Buck Institute for Research on Aging/UC Berkley

Anastasiia Rudenko comes to us from Kyiv, Ukraine. She is currently majoring in Behavioral Neuroscience with a Minor in Computer Science at Pace University. Anastasiia is excited to aid in developing a new level of research opportunities in Neurobiology.

Media Partner:

Categories SRF

An SRF-sponsored new organization and Longevity Summer Camp

SRF is a proud sponsor of LessDeath and the Longevity Summer Camp! LessDeath is a new organization and event series dedicated to helping people join the Longevity Biotechnology industry through education, career and community strategizing, job opportunities, and more.

You don’t need a biology PhD to get involved! The industry needs many types of scientists, engineers, programmers, founders, technicians, operations experts and more. If you’re passionate about maximizing human health and lifespan, LessDeath’s mission is to help you find effective ways to contribute!

LessDeath’s Longevity Summer Camp will be hosted July 20th-24th in California. Our very own Vice President of Research, Dr. Alexandra Stolzing, will be one of the camp counselors. Visit the link below to learn more and to apply to the summer camp.

Follow them on Twitter: @LessDeath.org

Use of this Web site constitutes acceptance of the Terms of Use and Privacy Policy.

© 2022 SENS Research Foundation – ALL RIGHTS RESERVED

Thank you for Subscribing to the SENS Research Foundation Newsletter.

You can also

or

You can