Here be DRACOs

This post isn’t about ageing, but about viral infections, which represent a health concern for just about anyone, regardless of their age. While “banal” viruses like the flu one are in general not too much of a hassle to deal with (at least if you’re young and with a healthy immune system), some others are much more pesky: HIV and Ebola, for example, can easily kill you or at least make your life a living hell, and at the moment there are no cures or vaccines available (although the recent outbreak of Ebola in Africa has to my knowledge resulted into the development of some potential vaccines which are currently under trial). The list of killer viruses is longer than that, and it’s not to be forgotten that, if your immune system is compromised, even a flu can turn into something much more serious and kill you.

The way we have dealt with viruses thus far is that of immune stimulation: vaccines are a preventative measure that basically make your immune system aware of the potential threat by means of introducing a killed or weakened form of the virus in your body. In this way, the virus cannot cause any harm (although sometimes you might get some watered-down symptoms), and your immune system can get to know the new pathogen, producing the appropriate immune cells to attack it, which will stick around an be ready to spring into action if needed.

Unfortunately this isn’t the bottom line. We’re not able to produce vaccines for all viruses: for example, HIV has been eluding our attempts for decades, despite the efforts put into the research and the progresses made (mostly in terms of antiretroviral drugs, since at the moment there is no fire-sure HIV vaccine). Viruses have evolution on their side, and they often evolve in such a way that our countermeasures become useless: that’s why, for example, there’s a new flu vaccine every year—the flu virus mutates fast.

There exist antiviral drugs, though, that instead of stimulating the immune system, try to inhibit the development of the virus directly—unlike most antibiotics, drugs targeted to bacteria and meant to kill them—but these drugs are difficult to develop, again because of the fast rate of mutations of viruses and because viruses use the host’s cells in their reproductive process: in a nutshell, it’s hard to interfere with viral replication without also harming the patient’s healthy cells. Additionally, for different viruses you need to design different drugs, so it’s kinda messy.

Some time ago, though, while working for Draper Laboratory, Dr. Todd Rider came up with a brilliant idea that promises to be the viral equivalent of antibiotics: DRACO.

DRACO (or rather DRACOs, since there are many) stands for Double-stranded RNA Activated Caspase Oligomerizer, and its working principle is very simple to explain in layman terms: all viruses use the host’s cells to reproduce. Once they’re done reproducing, the cell is almost certainly going to die, so it’s lost. The vast majority of  viruses, while reproducing, leaves behind a “trail” of double-stranded RNA, which is exactly what DRACO uses to screw the viruses over: DRACO doesn’t try to kill the virus, or to stimulate immune response. DRACO has two main components: one that targets the dsRNA trail, and one that triggers apoptosis, or programmed cell-death (your cells regularly do that, and then are replaced by new ones). You may guess already what happens at this point: DRACO detects infected cells by targeting the dsRNA trail, and when it finds it, it triggers apoptosis, killing the cell (which would be lost to the virus anyway) and preventing the virus from replicating.

DRACO is not just a theory: DRACO has been used in live mice and in human culture cells, and it has cleared them clean of 15 different dsRNA viruses, leaving healthy cells alone and without any adverse effect or sign of toxicity. Maybe it sounds too good to be true, but if you don’t belive me, believe the facts: have a look at Draper Laborary’s announcement a year ago, at the Wikipedia page of DRACO and the scientific paper published in 2011 by dr. Rider and his team. Just Google “DRACO antiviral” and have a look at the results. Or last but not least, check the video of a talk given by dr. Rider himself at—guess where—SRF’s conference SENS6 in 2013 (audio is unfortunately a bit crappy, bear with it).


Now, while it hasn’t yet been tested on live humans, there’s all the reasons to believe that DRACO would be just as effective as it has been in cells and mice, and that it would blow into the hell where they belong all those pesky little suckers obsessed with taking your life—including, but not limited to, HIV.

At this point you might think that, since the drug is so promising, they must be doing more experiments and that there’s funding going into them and that we’re soon to be told about human trials.
Nope.

Unfortunately I can’t find the sources, but a while back I have read that the research funding coming from NIH (the National Institute for Health in the States) , which was the main (if not only) source of money for DRACO had either been cut or drastically reduced for some obscure reason.  A non-profit organization was thus put up by ordinary citizens, called The DRACO Fund, aiming to raise money to devolve to this particular research. A noble goal: according to dr. Rider, as little as 10 more years of research should be enough to make DRACO a commercially viable drug, putting an end to viral infections. Well, the organization existed since at least 2013, when their facebook page was created, but it didn’t last much longer past 2014: they received a legal order from Draper Laboratory asking them to shut the whole thing down, and saying that they had sufficient funding for research and they would thus no longer accept the donations that The DRACO Fund was collecting. Good if, as they said, they had enough funding to go on, but it’s hard to understand why would they send a cease and desist order to have The DRACO Fund shut down.
The website of The DRACO Fund no longer exists, and their facebook page, still online, is now called Killing sickness and it still supports DRACO, albeit my understanding is that they have been reduced down to a fan page, basically.

That’s not the whole story.
Some time ago I signed a petition (which I urge you to sign yourself, too) to push NIH and the White House to find funds for DRACO research, and recently I received an email update from the same petition. The update said that dr. Rider has left Draper Laboratory, and the news is as recent as May 29th, 2015. The author of the petition, Sabrina Montgomery, has been and still is struggling to find a new facility for dr. Rider to continue DRACO research and to get him the fundings that are needed.

I don’t know what’s going on behind the scenes, but I know that, given enough funding and attention from the general public and authorities, we could put a goddamn tombstone on HIV, Ebola, influenza, and a bunch of other viral diseases as soon as ten years from now. I understand that people prefer to share cat pictures and funny stuff on facebook, but perhaps it’s also the case to spread the word about something more important, too—something that one day might save your life or your dear ones’.

Bottom line: sign the petition, share it, tell your friends, and particularly if you live in the States, push your political representatives to do something about this. Get in touch with Sabrina Montgomery and see if you can help, if it’s possible to put up a larger organization to support DRACO, particularly now that Draper Laboratory doesn’t seem to be involved anymore and thus has no say on where funds come from.
Ten years from now we might be able to laugh in the face of HIV. Think about it.

News for MitoSENS?

A recently published article on ScienceDaily talks about research done on human fibroblast cells to put to test the so-called mitochondrial theory of ageing, according to which—in a nutshell— the abnormal mitochondrial function observed in aged humans is due to accumulation of mutations in mitochondrial DNA; this specific aspect of ageing could in principle be dealt with by implementing MitoSENS.

The news is, though, that according to this experiment it seems that mitochondrial DNA mutations don’t play that big of a role in the decline of mitochondrial function as thought; the researchers had at their disposal cells from young and elderly humans, and they observed that while the so-called mitochondrial respiration was expectedly lower in older cells than in young ones, the amoung of mutations wasn’t significantly different. Additionally, the researchers found out that by means of epigenetic regulation of the genes regulating glycine production in mitochondria, they were able to restore the respiratory function in the elderly cells.

This would seem to make MitoSENS useless, since it is all about addressing mutation-caused problems, but it is to be said that, from what I recall of my reading of Ending Aging, these mutations are quite rare (1% of your cells) even in old age, so perhaps it comes as no surprise that the researchers didn’t find any significant difference; I have no say as to whether or not they play a role in ageing. That’s all I can guess: I would recommend you have a look at Fight Aging’s article about it, or perhaps even the relevant paper published by the Japanese team led by professor Jun-Ichi Hayashi.

The bottom line, though, is the usual: we need to do more research. We need to establish beyond reasonable doubt the causes of ageing if we want to defeat it. No anti-ageing science is carved in stone yet, but every tiny piece of the puzzle that we add to the picture gets us closer to the moment when ageing will be finally under medical control.

The Science Times: “New Therapy Strips Cancer Cells of their Immortality”

I’m sure that some people think that the world of anti-ageing medicine is either really tiny and quiet or non-existent, but facts prove them wrong all the time. In particular, this article talks about a new cancer therapy that is reminiscent of WILT: it takes away the ability of cancer cells to grow indefinitely. As we’re used to hear, the treatment was tried on mice only, but since it works on mice, the article says, “we can look to the future for its application in humans”.

The difference between this therapy and WILT is, as far as my understanding goes, that while WILT provides that the telomerase/ALT genes be deleted from the whole body, this therapy targets cancer cells specifically, “uncapping” their telomeres. The result is the same: the cancerous cells lose their immortality and die off just like any other cell.

Dr. de Grey himself says in Ending Aging that he hopes that better ways than WILT come along to defeat cancer: shutting off telomerase/ALT production altogether in the body is a scary option, because without that, even non-cancerous cells are doomed: they’d die off much faster than normal, and so would we; we’d need to compensate for such an accelerated cell loss, and that too would be RepleniSENS’s job.
As far as I remember, de Grey’s concerns were that targeting cancerous cells specifically to deprive them of their telomerase-induced immortality would be too difficult, while deleting the telomerase/ALT gene would be easier. Hopefully research like this will pave the way for cancer treatments that are just as effective as WILT would be, but less risky.

Sciencealert: “drug that rejuvenates ageing muscle and brain tissue” identified

According to this article, “scientists have identified a drug that simultaneously makes ageing muscle and brain tissue in mice act young again. The research is in its very early stages, but this could represent the first step towards a treatment that restores youth to multiple parts of the body at once”. In my limited understanding, this is pretty much what RepleniSENS would be about: use cell therapy to replace cells that are not being automatically replaced, although I would have a hard time saying if this is how it is envisioned in the SENS platform or not—according to the article, stem cells would in this case be perked up by means of a drug called Alk5 kinase inhibitor. The drug, says David Schaffer from the Berkeley Stem Cell Centre in the US, is capable of rescuing “essential function” in both brain and muscle tissue of aged mice.
The article does point out that this isn’t the only aspect involved in the ageing process and others need to be taken into account as well; what strikes me the most, though, is that the article also says that “of course we’re a long way off that [having body capable of stay healthy and young indefinitely], but it’s pretty exciting to think that we’re finally beginning to understand how our body ages… and how to reverse the process “. It looks like that at least somebody sees the potential of rejuvenation for what it is, instead of seeing it as a catastrophe! And If you look at the bottom of the article, you’ll see that it’s not the only one about ageing and therapies against it.
I like where this is going. 🙂

NewScientist: “Pill of super-protective ‘heavy’ fat may be key to eternal youth”

Once again the article title is a bit too enthusiastic: the pill, assuming it works as it should, would protect only against one type of ageing damage, so it’s not the “key” to eternal youth, but it would be a good step forward, I guess.
“Mikhail Shchepinov, director of Retrotope, a biotech company based in Los Altos, California, wants eventually to slow down the ageing process. But he is starting with a related problem – treating the inherited movement disorder Friedreich’s ataxia, with which ageing shares a mechanism. They are both caused, in part, by a molecular attack on our cells. Shchepinov’s idea is to counteract this assault by reinforcing our cells’ defences, slowing the progression of this incurable disease. If it works, it should demonstrate that the approach is also suitable for tackling ageing.”
The full article is on NewScientist.