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.