Longevity News Digest
Why Tech Billionaires are Investing in Aging
Dear Future Centenarian,
Times are a changin™.
It may not be long before you will have to go to a museum to see a test tube. Laborious hit and miss biology research is rapidly being replaced by faster, cheaper, easier and more precise methods.
Soon we™ll see more and more qualified researchers going into biology¦ and specifically aging research. That™s because biology is boiling down to programming.
We have known for quite a while that the approximate 22,000 genes in each of our cells are basically software programs, and we are making exponential
gains in accelerating the information processes that cracking the genome code has unlocked. We also have new tools that allow us to actually reprogram our biology in the same way that we reprogram our computers.
That™s why I spend lots of time on artificial intelligence and gene therapy. Add synthetic biology and nanomedicine to the mix and you can imagine the possibilities. You can see why biotech companies are acting more and more like software startups.
Austen Heinz, CEO of Cambrian Genomics, a company that sells built-to-order DNA strands, says you can imagine what will happen if biotech becomes as easy as software to try and to test. An “explosion of biotech companies is coming,” he says.
What half serious high school or college can™t do some programming? Imagine the millions of potential biotech researchers who are skilled programmers. These days, you can order DNA online, crowdfund a genetic engineering project, or outsource experiments. We™re taking longevity research over the top folks.
None of this is lost on the Peter Theils or Larry Pages and Sergey Brins of the world. In fact, they saw this coming long before most.
Peter Theil was one of the early private financial supporters of real longevity research. Google funded Calico and put Ray Kurzweil in an influential position. We may be hearing big things from Craig Venter and Human Longevity before long. And I expect others to follow.
Need I again remind you to do everything you can in order to not be left behind?
Latest Headlines from Fight Aging!
Theorizing that the Brain is Destroyed by the Pulse – Monday, March 23, 2015
It is uncontroversial that the age-related deterioration of the vascular system leads to damage to the brain, causing cognitive decline and then dementia.
Progressive stiffening due to cross-links and calcification and inflammation-driven remodeling of blood vessel walls reduces structural integrity at the same time as it causes hypertension, raised blood pressure that puts more stress on those same blood vessel walls. This paper presents a novel way of looking at this contribution to the aging process.
There are, in fact, comparatively straightforward paths to therapies that can mitigate this contribution to the aging process, though at present their development is given far too little attention and support by the research community.
Firstly prevent and reverse loss of elasticity in blood vessels, such as by breaking down persistent cross-links, and secondly target the mechanisms of atherosclerosis responsible for remodeling blood vessel walls to suppress inflammation and clear plaques. Target the root causes and natural repair mechanisms should do much to clean up the rest of the issue.
Ceria Nanoparticles Enhance Autophagy – Monday, March 23, 2015
Autophagy is one of the cellular housekeeping processes responsible for promptly clearing out damaged proteins and cell components before they cause more harm.
Autophagic activity declines with age, in part due to a buildup of resilient metabolic waste in lysosomes, the organelles responsible for breaking down materials and structures for recycling. The SENS strategy for this contribution to degenerative aging is to aim to remove that waste in order to restore function.
Globally increased autophagy is also a factor in many genetic and other alterations shown to slow aging and increase healthy life span in laboratory animals. Thus some researchers are investigating ways to boost this form of cellular housekeeping, and there have been some interesting demonstrations over the years, such as restoration of youthful liver function in old mice. Here one research group finds that nanoparticles can spur greater autophagy.
Another Study to Argue that Tau is Primary and Amyloid Secondary in Alzheimer’s Disease – Tuesday, March 24, 2015
The struggle to show meaningful progress in treatment of Alzheimer’s disease via clearance of amyloid has fueled significant investment into alternative hypotheses regarding the disease process.
The biochemistry of Alzheimer’s – and the brain in general – is so very complex that at this point it is a challenge to say whether the issue is that it is intrinsically hard to produce a useful clearance therapy via the present approaches, or whether amyloid is the wrong target for best effect.
A leading alternative candidate is a different form of metabolic waste, neurofibrillary tangles made of an altered form of the tau protein. Here is one of a number of studies that point the finger at tau rather than amyloid accumulation as the primary source of pathology.
The “Aging Kills” Initiative – Tuesday, March 24, 2015
A number of the efforts undertaken by the ever industrious Alex Zhavoronkov of InSilico Medicine involve reaching out into new communities to educate and raise awareness on the need for longevity science and the prospects for developing the means to treat aging.
He was presenting at a computing hardware conference recently, for example, talking about the path to greater healthy life spans to people who have probably never given the subject much thought. In advocacy experimentation is always necessary: success is obvious in hindsight, but you never really know where you are going to find significant new support for the cause.
This, for example, is presently an effort to make inroads into the electronic music and information technology communities.
Who Funds Basic Aging Research in the US? – Wednesday, March 25, 2015
Here is an interesting post from the Buck Institute on sources of funding for fundamental research into aging, with tables listing the various contributing organizations.
While looking through the list, it is worth bearing in mind that for really early stage, high risk, novel research the largest sources are unavailable. NIA grants, for example, only become a possibility once you’ve actually made the initial breakthrough and have early proof that you have achieved something new.
This is a systematic issue in medical research, and it is why philanthropic donations are essential for progress. Few really important novel attempts to advance the state of the art are directly funded at the outset by large institutional sources like the NIA or large pharmaceutical companies, though there is certainly a lot of creative bookkeeping that takes place in larger laboratories in order to split off the necessary funds for early stage, prospective work.
Without that very early stage work there would be no progress, but most funding sources – public and private – act as though the prototypes they are willing to fund come into existence from nothing, as if by magic.
Education Correlates With Longevity – Wednesday, March 25, 2015
It is known that greater educational achievement is associated with greater longevity, and this is one facet of a web of related correlations between various measures of intelligence, wealth, and health.
To my eyes this probably all boils down to influences on the degree to which people look after the health basics over a lifetime: exercise, weight, and smoking are the most important factors under individual control.
Maintaining a good, healthy lifestyle in this sense certainly doesn’t require wealth, but it happens that wealthy communities and networks do better than their less wealthy counterparts. People tend to adopt the culture that surrounds them.
Further Investigations of Neuropeptide Y and the Hypothalamus in Calorie Restriction – Thursday, March 26, 2015
A number of lines of research suggest that the benefits of calorie restriction for health and longevity largely derive from increased cellular housekeeping processes such as autophagy.
For example, the calorie restriction response requires neuropeptide Y (NPY), and here researchers explore the linkage of NPY with autophagy. They suggest that the role of autophagy in calorie restriction is indirect, and that it is a lynchpin part of the process only because a portion of the brain involved in the global control of metabolism responds to the level of autophagic activity.
A New Era of Aging Research – Thursday, March 26, 2015
Using the recent development of killifish as a model organism as a starting point, this popular science article looks at some of the more recent high profile developments in the study of aging.
It largely takes the longevity dividend party line of talking about extending healthy life span without extending overall life span, however. This is probably an impossible goal, and not even a desirable goal in comparison to extending both measures, but one that is politically easier to sell for various reasons.
So there is no discussion of approaches leading to rejuvenation and the prospects for radical life extension here. This gap in the conversation is a persistent remnant of the recent past in which researchers were very reluctant to talk about or attempt to work on any form of intervention in aging.
Leucine Supplementation as a Sarcopenia Treatment – Friday, March 27, 2015
The systematic loss of muscle mass and strength with age is given the name sarcopenia.
One of the potential contributing causes involves progressive dysfunction in processing of the amino acid leucine, and this might in theory be partially offset by leucine supplementation in the diet. This meta-analysis of past studies indicates that as a treatment it modestly improves muscle mass but not strength.
Myostatin Insufficiency Produces 15% Life Extension in Mice – Friday, March 27, 2015
Targeting myostatin and related biochemistry is well demonstrated to increase muscle mass and strength in mammals such as laboratory mice.
There are even rare natural mutants, including a few cows and humans, who lack normal myostatin and are as a result exceptionally strong in comparison to their peers.
Here researchers show that loss of myostatin mutations in mice produce extended life spans, but too much suppression of myostatin may remove that benefit due to the cardiac issues that can accompany an overly large heart.
Read More https://www.fightaging.org/archives/2015/03/myostatin-insufficiency-produces-15-life-extension-in-mice.php
DISCLAIMER:Â News summaries are reported by third parties, and there is no guarantee of accuracy. This newsletter is not meant to substitute for your personal due diligence and is not to be taken as medical advice. For originating report, please see www.fightaging.org/
David A. Kekich
Maximum Life Foundation
“Where Biotech, Infotech and Nanotech
Â Â Â Â Meet to Reverse Aging by 2033”