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Crowdfunding the Cure for Aging

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Senolytics – Taking Out The Trash Might Keep You Fit And Healthy

 

From around age forty we start to lose muscle mass due to various aging processes, one of these processes is the accumulation of senescent cells. Senescent cells are simply cells that have become damaged or have reached their maximum number of divisions. Normally these cells are shut down by a kind of self destruct program inside the cell, ready to be disposed of by the immune system.

 

However as the immune system ages, it stops clearing house properly, leaving many of these senescent cells in place. This would not be such a big deal, but senescent cells actually send out toxic inflammatory signals that block tissue regeneration. This includes the compromised formation and repair of muscle tissue[1-2]. Some researchers suggest that removing senescent cells could potentially lead to better performance and extending peak, allowing you to enjoy sports and remain competitive for longer.

 

There have been some interesting results on cardiovascular health and performance seen in pre-clinical studies so far. In tests aged mice had significantly improved vascular health when treated, compared to control mice left to age normally[3-4]. Perhaps even more exciting is the discovery that this therapy can also make an impact on heart disease. So reducing senescent cells could be a route to better cardiovascular health and improved fitness as we get older[5].

 

The name of compounds that can remove senescent cells are known as Senolytics and this video shows how they work:

 

 

So isn’t this like steroids?

 

Steroids are drugs that mimic certain natural hormones in the body that regulate and control how the body works and develops. Anabolic steroids are often used for sports, mainly because they are similar to the male hormone testosterone and they can improve endurance and performance, and stimulate muscle growth. Some people take anabolic steroids to help build muscles or to improve how they perform at sports, such as running and cycling. However using steroids is known to carry a variety of health risks.

 

Removing senescent cells from the body is nothing like this. It is really just helping the body to clear out the junk it struggles with as we age, and optimise its natural repair functions. Your body is designed to maintain a delicate balance known as homeostasis, but as you age that balance is gradually lost, what science is trying to do is help you to keep that balance and peak performance for longer.

 

The clues are already in nature

 

You have likely heard the phrase “An apple a day keeps the doctor away”, but there could be more truth to this saying than you might think.

 

Quercetin, one of the compounds that some studies suggest can remove senescent cells, is naturally found in apples and other fruits and vegetables [6-7]. An apple contains around 4.4 milligrams of quercetin for every 100 grams of apple. With a medium-sized apple being typically around 150 grams, it could contain up to 10 milligrams of quercetin. However to get a similar dose used in these studies for health purposes you would need to eat fifty apples a day!

 

Obviously unless you really like apples a lot this is completely impractical. This is why researchers have extracted pure quercetin from these foods, and it can be obtained cheaply as a dietary supplement with an effective and safe dosage.

 

So really, there could be some truth in the old saying about apples, after all.

 

Improving your body’s natural balance to maintain health

 

That said, there is always room for improvement. What science is doing now is investigating why these natural substances help your body maintain balance, and finding ways to improve upon this. The hope is that the longer your body can maintain homeostasis the longer you can enjoy your favorite sports, hobbies and benefit from an independent and active life.

 

As is the case in science there are of course no certainties, more studies need to be made before we can be sure these results will translate. However some will be entering human clinical trials in the near future so answers should not be too far behind. Companies like Unity Biotech, Oisin Biotechnology and Cellage are busy developing improved versions of these first pass therapies to make them even more effective and safe.

 

Hopefully we can all look forward to a healthier life thanks to progress like this, only time will tell.

 

 

 

 

 

 

 

Literature

 

[1] Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., Van De Sluis, B., … & van Deursen, J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 479(7372), 232-236.
[2] Sousa-Victor, P., Gutarra, S., García-Prat, L., Rodriguez-Ubreva, J., Ortet, L., Ruiz-Bonilla, V., … & Perdiguero, E. (2014). Geriatric muscle stem cells switch reversible quiescence into senescence. Nature, 506(7488), 316-321.
[3] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.
[4] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging Cell, 15(5), 973-977.
[5] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.
[6] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.
[7] Hollman, P. C., van Trijp, J. M., Buysman, M. N., Mengelers, M. J., de Vries, J. H., & Katan, M. B. (1997). Relative bioavailability of the antioxidant flavonoid quercetin from various foods in man. FEBS letters, 418(1-2), 152-156.

 

 

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Exciting Potential For Twin Therapy To Destroy Cancer

The clearance of senescent cells has been receiving a great deal of attention in the last year or so, and quite rightly so given the impressive results thus far. As the body ages cells become damaged and cease dividing entering a state known as senescence. Normally these senescent cells destroy themselves through a programmed cell destruction mechanism known as apoptosis and the immune system then clears them away.

Unfortunately as we age an increasing number of these cells escape this process as cellular signalling and the immune system become dysfunctional. These zombie cells remain in the body. The problem is they then produce a range of toxic signals that cause inflammation, can even affect healthy neighboring cells[1-2], and increases the risk of cancer[3] and other diseases[4-5]. In tests with mice when these cells were removed it led to an increased period of health[6]. Fortunately a new class of drugs are able to remove these toxic dysfunctional cells from the body, they are known collectively as senolytics[7-8].

Today we have another example of the direction researchers are moving in regards to using these senolytic therapies for the treatment of diseases, in this case cancer is the focus. Perhaps more interestingly researchers in this review not only propose to use Senolytic therapies, but combine them with another new type of cancer treatment, “pro-senescence” therapy.

As we recently reporteda strong connection between senescent cells and cancer relapse after chemotherapy has been established. Chemotherapy not only kills cancer cells, but also does a great deal of damage to surrounding healthy cells and turns them senescent increasing the risk of relapse[9].

In contrast to normal cells, one of the hallmarks of cancer cells is the capability to escape senescence, thus acquiring a limitless replicative potential that is the prelude to invasion, metastasis and additional features of malignancy. However, cancer cells can undergo senescence if subjected to certain insults such as oncogenic stress, DNA damage and metabolic changes. This type of senescence response occurs immediately and also independently of telomere shortening, a phenomenon known as “premature” senescence. For instance, several anticancer chemotherapies and radiotherapies are known to induce senescence in both normal and cancer cells. Senescence can also occur in tumour cells in vivo as a consequence of overexpression of oncogenes or loss of tumour suppressor genes, demonstrating for the first time that senescence acts as a barrier against tumorigenesis. Analysis of tumour samples from patients demonstrated that, whereas benign tumours accumulate markers of senescence, invasive cancers lack senescence. Subsequent publications validated these findings in different types of tumour. Given the surprising discovery that senescence limits the development of cancer, we and others envisioned targeted therapies that selectively enhanced senescence in cancer cells used for the therapy of various tumours. This approach, named “pro-senescence” therapy for cancer, differs from the chemotherapy-induced senescence that affects both normal and cancer cells.Several small molecule inhibitors that are currently in clinical development have been reported to induce senescence in cancer. Among these compounds, inhibitors of the cyclin-dependent kinases CDK4/6 have been associated with a high percentage of responses in patients affected by breast cancer and are the most promising pro-senescence compounds currently being tested in the clinic. Compounds that enhance the level of the tumour suppressor gene p53, such as MDM2 inhibitors and PRIMA-1 analogues, have been reported to enhance senescence in tumour cells with normal and mutant p53 and are currently being tested in the clinic. Many compounds that are currently being tested at the preclinical level are also promising pro-senescence therapies. Inhibitors of SirT1, a protein deacetylase that negatively regulates p53 function in cancer, induced senescence in preclinical tumour models. MYC inhibitors can also drive a cellular senescence response.

Source: Swiss Medical Weekly

However as exciting as a dual therapy approach is, and exactly the kind of revolution in medicine we need, there are technical problems to overcome. The accurate detection of senescent cells is a real problem for researchers, and traditional methods to measure them using SA-β-galactosidase is not good enough[10].

Another challenge in the field of senescence therapy for cancer is the lack of clinically validated biomarkers for the identification of senescence in human tumours. The prognostic use of senescence-associated-β-galactosidase (SA-β-galactosidase), a well characterised in vitro marker for senescence, has been tested in small trials evaluating the efficacy of neo-adjuvant chemotherapies. Results from these trials demonstrate that this marker increases upon treatment and predicts patient outcome. However, the use of SA-β-galactosidase alone as a unique marker of senescence has been criticised since it can lead to many false positives. Recent findings have identified of new markers of senescence with prognostic relevance. However, neither SA-β-galactosidase staining nor additional markers have been used so far in large clinical trials to evaluate the efficacy of pro-senescence compounds. Thus, development of novel biomarkers that can accurately assess the occurrence of senescence in cancer patients is the need of the hour. This would help improve the stratification of patients who may respond to therapies that enhance senescence in cancer.

Source: Swiss Medical Weekly

Combination therapies that include both Senolytic and Pro-Senescence therapies are a compelling direction to advance cancer treatment. It is quite reasonable to believe in a few years these will become the standard of care, replacing harsh chemotherapy and improving patient outcomes.

 

Literature

[1] van Deursen, J. M. (2014). The role of senescent cells in ageing. Nature, 509(7501), 439-446.
[2] Freund, A., Orjalo, A. V., Desprez, P. Y., & Campisi, J. (2010). Inflammatory networks during cellular senescence: causes and consequences. Trends in molecular medicine, 16(5), 238-246.
[3] Coppé, J. P., Desprez, P. Y., Krtolica, A., & Campisi, J. (2010). The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual Review of Pathological Mechanical Disease, 5, 99-118.
[4] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.
[5] Xu, M., Bradley, E. W., Weivoda, M. M., Hwang, S. M., Pirtskhalava, T., Decklever, T., … & Lowe, V. (2016). Transplanted senescent cells induce an osteoarthritis-like condition in mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glw154.
[6] Baker, D. J., Wijshake, T., Tchkonia, T., LeBrasseur, N. K., Childs, B. G., Van De Sluis, B., … & van Deursen, J. M. (2011). Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature, 479(7372), 232-236.
[7] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.
[8] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging cell.
[9] Demaria, M., O’Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., … & Alston, S. (2016). Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse. Cancer Discovery, CD-16.
[10] Matjusaitis, M., Chin, G., Sarnoski, E. A., & Stolzing, A. (2016). Biomarkers to identify and isolate senescent cells. Ageing research reviews, 29, 1-12.

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New Cell Therapy Could Help Fight Cancer

Lately the focus has been on the removal of senescent cells as a therapy to treat age-related diseases by directly addressing one of the processes of aging – senescent cell accumulation. Senescent cells are simply cells that have become damaged or have reached their maximum number of divisions. Normally these cells are shut down by apoptosis, a kind of self destruct program in the cell ready to be disposed of by the immune system. Unfortunately as we age more and more of these cells accumulate and they cause inflammation and contribute to various age-related diseases such as, atherosclerosis[1], osteoporosis[2][3] and cancer. The removal of these cells has been suggested as the solution to this problem and it has the potential not only to increase the period people spend healthy but also improve patient outcomes for chemotherapy.

 A new research paper hot off the press shows another connection that in retrospect should have been obvious, the connection between cellular senescence, cancer[4] and the side effects of chemotherapy[5].

Chemotherapy is extremely toxic and damages and deregulates a number of cellular functions in the body, the therapy works by inducing cancer cells to become senescent, but this process also causes a great deal of collateral damage that stresses healthy cells too and causes a significant number of them to become senescent. These populations of senescent cells are already accumulating naturally as part of the aging process anyway and chemotherapy increases their numbers even more. In a very real sense, a course of chemotherapy could be considered accelerating this particular aspect of aging.

Senescent cells do not divide or support the tissue they are a part of, but instead emit a range of potentially harmful chemical signals, these encourage other nearby cells to also enter the same senescent state. Their presence causes many problems: they degrade tissue function, increase levels of chronic inflammation, and can increase the risk of cancer as this latest paper discusses.

 

Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse

Abstract

Cellular senescence suppresses cancer by irreversibly arresting cell proliferation. Senescent cells acquire a pro-inflammatory senescence-associated secretory phenotype. Many genotoxic chemotherapies target proliferating cells non-specifically, often with adverse reactions. In accord with prior work, we show that several chemotherapeutic drugs induce senescence of primary murine and human cells. Using a transgenic mouse that permits tracking and eliminating senescent cells, we show that therapy-induced senescent (TIS) cells persist and contribute to local and systemic inflammation. Eliminating TIS cells reduced several short- and long-term effects of the drugs, including bone marrow suppression, cardiac dysfunction, cancer recurrence and physical activity and strength. Consistent with our findings in mice, the risk of chemotherapy-induced fatigue was significantly greater in humans with increased expression of a senescence marker in T-cells prior to chemotherapy. These findings suggest that senescent cells can cause certain chemotherapy side effects, providing a new target to reduce the toxicity of anti-cancer treatments.

In conclusion chemotherapy causes the rapid accumulation of senescent cells and ultimately in the long run is bad for the patient due to driving this aging process and the risks that entails. However until alternatives such as Immunotherapy arrive, senolytic therapies could help to reduce the negative impact of chemotherapy while we wait for better things to replace it. 

 

Literature

[1] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.
[2] Farr, J. N., Fraser, D. G., Wang, H., Jaehn, K., Ogrodnik, M. B., Weivoda, M. M., … & Bonewald, L. F. (2016). Identification of senescent cells in the bone microenvironment. Journal of Bone and Mineral Research, 31(11), 1920-1929.
[3] Xu, M., Bradley, E. W., Weivoda, M. M., Hwang, S. M., Pirtskhalava, T., Decklever, T., … & Lowe, V. (2016). Transplanted senescent cells induce an osteoarthritis-like condition in mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glw154.
[4] Coppé, J. P., Desprez, P. Y., Krtolica, A., & Campisi, J. (2010). The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual review of pathology, 5, 99.
[5] Demaria, M., O’Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., … & Alston, S. (2016). Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse. Cancer Discovery, CD-16.

 

 

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Will synthetic biology help us to treat age-related diseases?

All living organisms contain an instruction set that determines what they look like and what they do. These instructions are encoded in the organism’s DNA within every cell, this is an organism’s genetic code (or “genome”).


Mankind has been altering the genetic code of plants and animals for thousands of years, by selectively breeding individuals with desired features. Over time we have become experts at viewing and manipulating this code, and we can now take genetic information associated with the desired features from one organism, and add it into another one. This is the basis of genetic engineering, which has allowed us to speed up the process of developing new breeds of plants and animals.

More recent advances however have enabled scientists to create new sequences of DNA from scratch. By combining these advances in biology with modern engineering, chemistry and computer science, researchers can now design and construct new organisms with cells that perform new useful functions. This “customised” cell biology is the essence of synthetic biology.

 

Ok, but what can we use it for?

 

Synthetic biology aims to make the biology of an organism easier to engineer using a combination of chemistry, biology, computer science and engineering. This enables researchers to turn an idea into a product faster, cheaper, and with greater precision and safety than ever before.

It could be used to drive down the cost of production for a variety of things such as making cells that produce biofuels, secrete chemicals used for medical drugs, create better crops resistant to drought or pests. It perhaps it could even improve the cells in our own body to better resist damage and stay healthier for longer.  

Perhaps even more importantly we could use genetic circuits created by means of synthetic biology to treat age-related diseases by removing the toxic senescent cells from human body. These cells accumulate in the body as we age and contribute to heart disease[1], cancer[2], osteoarthritis and other serious conditions[4]. So targeting and removing them could help us to maintain a healthier and more independent life as we get older.  


So, how does it relate to health?

 

Companies like CellAge are working on synthetic biology with a specific focus on medical application: using scratch built genetic constructions to detect and remove senescent cells from the body.


The technology could be used to help improve stem cell therapies. Being able to sense and remove senescent cells before transplant to a patient would improve quality control for better patient outcomes.

It could also help reduce the chance of relapse from chemotherapy where the damage from chemo causes many otherwise healthy nearby cells to become senescent[5].

Being able to detect these cells has wider potential too, if researchers can spot these problem cells it can help them determine if new drugs are effective and speed up new drug discovery.

This technology could even be used to determine how fast someone is aging making it an excellent general diagnostic for monitoring health. This would be especially useful for knowing when best to apply senescent cell removal to effectively prevent age-related diseases from developing.

So really synthetic biology opens up a world of exciting possibilities, offering us new tools that could help to keep us healthier and enjoying life for longer.


Literature
[1] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.
[2] Campisi, J. (2005). Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors. Cell, 120(4), 513-522.
[3] Xu, M., Bradley, E. W., Weivoda, M. M., Hwang, S. M., Pirtskhalava, T., Decklever, T., … & Lowe, V. (2016). Transplanted senescent cells induce an osteoarthritis-like condition in mice. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, glw154.
[4] Freund, A., Orjalo, A. V., Desprez, P. Y., & Campisi, J. (2010). Inflammatory networks during cellular senescence: causes and consequences. Trends in molecular medicine, 16(5), 238-246.
[5] Demaria, M., O’Leary, M. N., Chang, J., Shao, L., Liu, S., Alimirah, F., … & Alston, S. (2016). Cellular Senescence Promotes Adverse Effects of Chemotherapy and Cancer Relapse. Cancer Discovery, CD-16.

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CellAge 1-month campaign extension announced

While the CellAge campaign has done a great job thus far, with over 200 backers raising $11,000+ to better target dysfunctional “senescent” cells in the body, many supporters have let us know that the holidays, along with other concurrent fundraisers, have made it challenging to contribute.

 

In response we have decided to announce a 1-month extension for the CellAge campaign, and give the generous members of our community greater opportunity to support this important research.

 

If you are unfamiliar with the project: CellAge is developing tools to better target and remove harmful senescent cells that accumulate in the body with age and play a role in various diseases such as heart disease, cancer, and osteoarthritis, and which also complicate recovery after certain treatments like chemotherapy. Having the ability to selectively remove these cells is a critical component in the fight against age-related diseases and an important tool towards lifespans that are both long and healthy.

 

Having the ability to selectively remove these cells is a critical component in the fight against age-related diseases and an important tool towards lives that are both long and healthy.

 

If you would like more in-depth information about the project you can visit the campaign page, read this Ask-Me-Anything on Reddit, or watch these videos from the CellAge  project creator answering some commonly asked questions.

 

Thank you for your support thus far. We have a lot of exciting initiatives on the horizon, so let’s make 2017 the year we really move the needle on aging research.

 

 

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The #LifespanChallenge Starting on October 1 — International Longevity Day

Over the past few years there has been a tradition emerging of longevity researchers and activists around the world organizing events on or around October 1 — the UN International Day of Older Persons, or Longevity Day.

This is an excellent idea, and to take it further Lifespan.io will be running a social challenge campaign, not unlike the Ice Bucket Challenge, to raise both funds and awareness for life extension research — the #LifespanChallenge. It will begin on October 1 and run through the month of October.

— The Challenge —

  1. Donate any amount via Lifespan.io to a running campaign or to the Life Extension Advocacy Foundation (LEAF). If you have already done so already, feel free to skip to the next step.
  2. Post a short video (or image with description) on social media where you:SignGroup1
    1. are holding up the #LifespanChallenge sign (which you can print or show on a tablet, etc.)
    2. share a personal reason why you sincerely care about life extension, or express yourself in any way that is linked to this theme
    3. challenge 3 friends to do the above as well
  3. Add a post description similar to this:
    “Hey everyone; here is my response to the #LifespanChallenge to help extend healthy lifespan! My reason for helping this cause is _____.   If you want to help please donate any amount to https://www.lifespan.io/donate/ or projects at https://www.lifespan.io, do a video like this, and challenge 3 of your friends to do the same. For example @FriendName1, @FriendName2, @FriendName3 I challenge you!”

— Tips —

  1. Facebook has made it easy to upload video directly, so all you should need is a cell phone camera.
  2. The text that accompanies your post should be informative, tagging your friends (preface their name with an @ in Facebook, for example) and including the hashtag #LifespanChallenge.  This will make the post visible to your friends and easy to find later.
  3. One of the goals of this challenge is to introduce more people to the idea of life extension, so make it a point to talk to at least one friend who is not already part of the life extension community about the #LifespanChallenge, and open up a dialogue around this topic.
  4. Don’t wait to be challenged; be a part of the first wave and help really get the ball rolling.

That’s it! Let’s keep up the momentum to #CrowdfundTheCure, and I hope you all have an excellent Longevity Day. Special thanks to the enthusiastic supporters who created and held up signs when we first launched (examples below); it was you who gave us the idea for the #LifespanChallenge.

——Keith

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The Lifespan.io Launch is Here — Let’s #CrowdfundTheCure for Aging!

After many long nights and much hard work, we are excited to announce the launch of Lifespan.io — a platform dedicated to funding and raising awareness for research aimed at extending healthy human lifespan. We believe that by centralizing crowdfunding efforts in this space we can build a powerful network of researchers, donors, and supporters that can seriously move the needle on accomplishing this important humanitarian goal.

To begin this process, we are pleased to be working with the SENS Research Foundation in support of their project to repair mitochondrial damage, and thus help defeat some truly terrible diseases. Please support their campaign, and remember that by doing so you are not just aiding this one institution, but also empowering a growing grass roots movement to cure the diseases of aging, and having direct agency in the progression of life saving therapies.

We are proud to be working with our launch teams, our Scientific Advisory Board, and hopefully you as well. Donate if you are able, and please share this post and our campaigns with the hashtags #crowdfundthecure and #LifespanIO to spread the word. Let’s send a powerful message that the public can come together and meaningfully act on this issue of healthy aging, which truly affects us all.

Whatever your particular thoughts on life extension may be, no one wants diseases like Alzheimers or to see their loved ones in pain with the passage of time. Let’s work to decouple such suffering from the concept of aging. Together, we can #crowdfundthecure for aging. Thank you.

——Keith

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