Update bundle #4

Gone are—for now—the golden days when I would publish a new post each week. So, for as long as my schedule is going to be this busy, I’ll have to be content with update bundles. I thought I’d let you know about a few news items and interesting things going on in anti-ageing community.

News from LEAF

On June 30 LEAF will host their first Journal Club event, with dr Oliver Medvedik. The topic will be the implications of epigenetic alterations on aging and as a primary aging process.

The recurring crowdfunding campaign to support LEAF has reached $1110, thus surpassing the first goal of $1000. The next one is $2000, and it’d be great if you could help us reach it, and advertise the campaign so that others may help too.

Another way you can help is by becoming a volunteer—there’s never a shortage of stuff to do in the world of anti-ageing research advocacy, and your talents may be precious. You can also join the community on discord to find out what’s going on and how you can help.

Keep an eye on LEAF, because new campaigns are to be expected fairly soon.

The state of the art

Rejuvenaction does a lot of rejuvenation advocacy, but doesn’t talk much about rejuvenation science. That is on my to-do list and is going to change; for the time being, here’s a brief update on a few research projects, categorised for simplicity the SENS way. None of these is exactly news, but they may give you an idea of where we are in terms of progress, in case you have been out of the loop.

LysoSENS

Clearing up the indigestible junk that accumulates in our lysosomes as we age is crucial in the fight against age-related diseases. The SENS approach to the problem of lysosomal dysfunction consists in upgrading our lysosomes with genes that allow them to produce enzymes that break down the previously unbreakable. A first example of this type of therapy moving towards the clinic is that of LysoCLEAR, an enzyme product in the pre-clinical trial stage specifically tailored to treat age-related macular degeneration (AMD) and its early onset version, juvenile macular degeneration. AMD is one of the leading causes of blindness among the elderly; if successful, LysoCLEAR would not only help old and young alike get back their sight, but it could also pave the way to similar treatments for lysosomal dysfunction in different tissues of the body. Indeed, while LysoCLEAR is targeted to treat the macula, its creator Kelsey Moody is optimistic that the method behind LysoCLEAR can be adapted to target different tissues.

This is not exactly full-scale LysoSENS yet—because we’re not talking of inserting new genes anywhere but rather of a treatment based on enzyme replacement therapy—but it’s an excellent step forward and it definitely is a maintenance-based approach which, at the end of the day, clears out unwanted junk. I suppose it can be seen as a ‘manual’ version of LysoSENS, since the necessary enzymes to clear up the macula aren’t produced directly by the body but are delivered by the drug itself.

Another project, a joint effort by SENS Research Foundation and the Buck Institute for Research on Aging, may help us get to the ‘automatic’ version of LysoSENS. The goal of the project is testing out an improvement on somatic gene therapy that uses CRISPR to control where specific genes are added to the genome. Further coverage can be found on FA! —which I always recommend as your primary source for anti-ageing science, together with LEAF. (See Jim’s comment below for a clarification.)

ApoptoSENS

Another cause of pathology in old age is the accumulation of senescent cells—cells that should die, but do not have the decency to do so. These felons have stopped replicating entirely, but don’t die. Instead, they stick around and secrete harmful chemicals. Their existence is a bit of a trade-off: They’re useful in small amounts (they play a role in wound healing and help preventing cancer), but once we hit old age they’ve built up to intolerable amounts, and far from being a solution, they become a problem. That’s why they’re one of the primary targets of ApoptoSENS.

In the past few years, senolytics—drugs capable of targeting and destroying senescent cells—have been often in the spotlight among the anti-ageing research community. Several biotech companies, such as Oisin, Unity, and CellAge, are working on different types of senolytics to get rid of excess senescent cells. The Life Extension Advocacy Foundation ran a rather successful crowdfunding campaign for CellAge last year, and Unity’s senolytics are supposed to enter clinical trials in 2018. Additionally, SENS Research Foundation and the Buck Institute for Research on Aging have recently joined forces on a research project focussed on the clearance of senescent cells in the immune system, led by renowned expert Professor Judy Campisi.

Methuselah Foundation’s new fund

Earlier this year (I told you I’m a slow poster) Methuselah Foundation launched the Methuselah Fund, aimed at providing financial help for promising scientific teams that would like to launch their own company focussed on rejuvenation biotechs. Professional investors’ interest is definitely welcome, and you can get in touch with sergio@methuselahfund.com if you’re interested; however, participants to the Methuselah 300 can complete their pledge by investing in the Methuselah Fund as well.

Upcoming MMTP Longevity Panel

MMTP will host a panel with dr. Alexandra Stolzing, dr. Aubrey de Grey, and other guests in early June—the exact date is to be confirmed. The panel will be livestreamed on Facebook and is offered as one of the rewards for donating to MMTP’s fundraiser on Lifespan.io in 2016. If you have any question to for Alexandra or Aubrey, or the other guests, be sure to submit it to info@majormouse.org.

Advancing Conversations with Aubrey de Grey

If you want an inexpensive, lightweight book that discusses the key points of the rejuvenation cause, either for your own reading or to recommend to others who aren’t willing to go through Ending Aging, I suggest you take a look to Douglas Lain’s Advancing Conversations: Aubrey de Grey—Advocate for an Indefinite Human Lifespan. It’s short, not sciencey and thus simple to read, and it answers quite a few questions that a newbie to the cause may have.

Update bundle #3

Last update: 20.01.2017.

Happy New Year! Yes, I realise I’m a bit late for that one, but I’ve been quite busy in the last month. I spent good part of my Christmas holidays and of January working on some improvements to Rejuvenaction, and yet others are planned. Let me tell you about them.

The largest change is the new version of the overpopulation objection. I’d been wanting to revise it for some time already, and I added a lot more meat to it in the process. I split it into three separate sections dealing with different aspects of the problem; each of them goes much more into detail than before. Comments and suggestions are welcome, especially if you notice any mistakes that I may have overlooked.

I answered two more objections, namely Rejuvenation will be too expensive to create and Rejuvenation won’t happen within my lifetime.

I also created a page containing all answers in short, whose purpose should be self-explanatory. Each short answer on this page links to the corresponding full answer both on Rejuvenaction and LEAF (if available). More generally, each time you see this icon

leaf

it means the article you’re reading has a counterpart on LEAF which I linked to and you may want to check out.

I also retouched some other articles here and there, and shortened the titles of menu items for the sake of navigability. Should you find any broken links anywhere, please let me know. With all the changes I made, it’s bound to have happened somewhere.

Next, I’m planning to add more content to the section about ageing and SENS, but it’ll take a while before I even begin, so don’t hold your breath.

On an unpleasant note, the crowdfunding campaign for CellAge has only two days left to go and has reached only 29% of the goal. If you can help push that percentage a bit higher, please do.

UPDATE: The CellAge fundraiser has been extended until February 24th, and is currently 30% funded. We’ve got over a month’s time to make it 100%!

Update bundle #2

It’s been quite a while, and my schedule is no less hectic than before, unfortunately. I cannot yet get around shortening my to-post list, but I can’t help writing something about some good and important news.

Lifespan.io’s crowdfunding project for MitoSENS: When the campaign started, on August 25th, I didn’t know what to expect, and I probably wasn’t expecting much at all. However, much to my delight, about ten days later, roughly 40% of the 30.000$-goal was already pledged, and now, twenty-six days before the end of the campaign, the project is 102% funded (so there is almost one more month to make that percentage grow even higher). It’s a clear sign that people are becoming more and more aware that ageing is a medical problem that we can and must address.

FightAging!’s matching fundraiser starts on October 1st: FA!’s annual fundraiser is set to start tomorrow, This year’s matching fund amounts to 125.000$, so for every 1$ you donate, 1$ will be unlocked form the fund; the goal is to raise a grand total of 250.000$ by the end of the year. Let’s all help to make this goal come true—remember, every donation counts, however small.

Killingsickness’ Indiegogo campaign: On October 6th, Killingsickness will launch their crowdfunding campaign to finance research on DRACO, a broad-spectrum antiviral drug that holds the promise of putting an end to nearly all viral diseases. You can join their mailing list to keep up-to-date with their progress and news.

UPDATE : I had forgot something.

Lifespan.io’s longevity challenge: Lifespan.io challenges you to help the cause either by donating or by publishing a picture or video on your social media to tell your friends why you care about healthy lifespan extension. The challenge will last for the whole month of October.

Update bundle #1

These days I am quite busy with several projects, leaving me little time for anything else, so my list of things I wanted to post about is growing longer and longer. I resolved that I need to establish which items on the list deserve a post of their own, and which ones can be grouped together in a single bundle; it could get a bit messy, but at least I will be able to post the news before they become too old. Therefore, here comes the first update bundle. Where applicable, I will cite a brief excerpt from every linked article, but I do recommend you go and give a look to them in their entirety.

 
Fight Aging!’s fundraiser
I’m pleased to see that the fundraiser has reached a total of $70,000. I have no doubts that we can do even better 🙂

 
Quest to redefine ageing
NOVATO — Death will come; that we know. But as each of us traverses a path toward inevitable demise, the length of the path matters less than the quality of the trip and its cost in pain and dollars. In the past year, business interest in aging research has surged. The potential payoff in profits and quality of life is staggering.

As a sidenote, I would like to point out that if we cure ageing comprehensively, then death’s come is not all that certain anymore, because just being mortal doesn’t mean that you will die, but only that you can die.

 
SENS: Are Mitochondrial Mutations Really All That Important?
You might recall that I posted about a recent study that seemed to question the importance of mitochondrial mutations in ageing. SENS has written an article about the study; I recommend you follow the link for all the details; what follows id a brief summary takesn from the source itself.

Q: A recent study out of Japan got a lot of coverage in the press, claiming to overthrow much of what was known about the role of mitochondria in aging. It is said to have found that mitochondrial mutations don’t really accumulate in aging cells over a lifetime. Instead, it found that age-related mitochondrial dysfunction is driven by “epigenetic” changes — changes in the “scaffolding” around DNA that helps regulate which genes are turned on and turned off. In particular, the investigators traced the effect back to the epigenetic downregulation of two genes involved in glycine production in mitochondria, such that providing them with glycine restored much of their normal function. Does this mean mitochondrial mutations really aren’t a problem and we can stop working to fix them?

A: The study is interesting, and contributes to a long-standing debate in this field about the frequency of specific mitochondrial DNA mutations with age and tissue type, and whether they contribute to specific diseases. It is clear at this point that michondrial dysfunction occurs with age and that damage in the form of mutations to mitochondria contributes to the diseases and disabilities of aging. We don’t believe that this particular study is actually a challenge to scientists’ existing understanding about how changes in mitochondria with age both drive and are driven by cellular and molecular damage, and the diseases and disabilities of aging. To maintain and restore youthful good health in aging people, it remains imperative to repair the cellular and molecular damage of aging directly, including alleviating the effects of large DNA deletions in aging mitochondria.

 
Team develops transplantable bioengineered forelimb in an animal model
A team of Massachusetts General Hospital (MGH) investigators has made the first steps towards development of bioartificial replacement limbs suitable for transplantation. In their report, which has been published online in the journal Biomaterials (“Engineered composite tissue as a bioartificial limb graft”), the researchers describe using an experimental approach previously used to build bioartificial organs to engineer rat forelimbs with functioning vascular and muscle tissue. They also provided evidence that the same approach could be applied to the limbs of primates.

 
New class of drugs dramatically increases healthy lifespan, mouse study suggests
A research team from The Scripps Research Institute (TSRI), Mayo Clinic and other institutions has identified a new class of drugs that in animal models dramatically slows the aging process — alleviating symptoms of frailty, improving cardiac function and extending a healthy lifespan.

 

That’s all for now.