First
DNA
extraction
of
O and B flies using a QPCR kit. Samples
were sent to Illumina for sequencing.
Started
testing
a resveratrol analog, Pine Bark extract, on
“B” flies at
the recommendation of Dr. Spindler at UCR. We tested varying doses
of Pine Bark extract alone and in combination with Uridine, which is
our negative control.
Spring
Quarter
Our
Gen5 experiment tested 3 doses of Pine Bark using the new non-yeast
drug delivery system.
The
low dose of Pine Bark demonstrated a minor increase in longevity.
Because
of ease of use and reduction of background statistical noise, we
decided that all substance testing going forward will use the new
non-yeast drug delivery system.
Our
Gen6 experiment was the first comparative mortality assay of the B
(27 days), O, and SO flies. SO lifespan (69 days) was found to not
be significantly longer than the O flies (67 days) after 2 years of
continued selective breeding.
Summer
Quarter
In our Gen7 experiment, we tested an early version of MX-100 for the first time.
We found that MX-100 increased the lifespan of our Wild-Type B flies by about 16%.
Fall
Quarter
In our Gen8 experiment, our lab tested a new formulation of MX-100 containing more astragalus extract, the lead active component.
MX-100 increased the lifespan of the B flies by about 65% in this experiment, and a late-life plateau was observed with about 10% of the population remaining.
Interpretation of genetic data from fruit flies bred for longevity suggests the major culprit [behind poor health, disease and limited healthspan] may not be accumulated damage, or any particular mechanism, but rather the intersection of biological complexity with evolutionary adaptation By Ben Goertzel
August 10, 2010
Excerpt from the August 10, 2010 H+ Magazine Editor’s Blog H+ Magazine (published online August 12, 2010)
Drosophila Melanogaster Photo: michael*
. . . Genescient’s . . . Chief Scientist (and professor at the University of California at Irvine), the evolutionary geneticist Michael Rose, advocates a perspective that takes biological complexity even more seriously. Like de Grey, he views health at a systems level, rather than looking for a single core mechanism underlying aging. But he doubts whether accumulated damage is the critical factor we should be examining.
Rose likes to highlight results showing that, after a certain age has passed, an organism’s death rate (its odds of dying during a given year) stop increasing. During this “late life” period, in a fundamental sense, the organism’s health may not be wonderful, but it’s not getting any worse. Of course, some body systems like human teeth might keep degenerating even during late life, but the point is that the apparent existence of a “late life” period with a constant (or near constant) death rate argues against the notion that accumulating damage gradually kills an old organism off.
In Rose’s view, as organisms evolve different genetic mutations arise to adapt the organism’s functionality at different stages of its life. But genes (considered as biological actors, not just sequences of amino acids) are complicated things. Each gene may carry out multiple functions, and in each of these functions, it’s subtly interlinked with other genes. So various adaptations, focused on different stages of life, may interfere with each other in complex ways — an instance of a phenomenon known in genetics lingo as “antagonistic pleiotropy.” And antagonistic pleiotropy causes the organism all sorts of problems. The more different life-stages worth of adaptations get piled on top of each other, the more confusion occurs in the body’s various interlocking systems, causing the problems we all experience as we age. When an organism gets old enough, it reaches an age for which there hasn’t yet been much evolutionary adaptation in its history. Few organisms in its species have lived that long, so the genes of the species haven’t adapted much to the requirements of life at that age. ‘
For instance, not many people have lived to age 100, so the human genome has not adapted much to the particular requirements of life at age 100. Because of this, the human body at age 100 doesn’t have a lot of new problems due to conflicting adaptations, beyond the problems already present in the body at age 90. On the other hand, many people have lived to age 50, and 40, and 30, etc. So a 50 year old human’s body is full of adaptations specialized to improve life at age 50, along with some specialized to improve life at age 40, and some specialized to improve life at age 30, etc. These different adaptations, specialized to improve life at different ages, often conflict with each other (e.g. because the same gene often serves multiple functions and plays roles in multiple networks), creating problems for the 50 year old, including many of the phenomena we describe as “aging.” In other words, at a certain age (somewhere between 50 and 100 years for humans), the problems experienced earlier in life stop compounding, and the death rate levels off.
If this is correct, then accumulated damage of the sort SENS seeks to address isn’t exactly irrelevant, but it no longer assumes a central role. Some accumulated damage may continue into late life, but it’s not a star in the drama of mortality. Rather, it is a bit player at best . . .
Irvine, CA, December 17, 2009 — Genescient Corporation, a California genomic-health biotechnology company, received $500,000 in new angel investment, to help commercialize the company’s technology and to fund further research.
The investment was made by private investors with an interest in the rapidly growing field of nutrigenomics, based on the science of epigenetics and its promise of healthy life extension. A spokesman for the investors, Douglas Arends, stated: “We are especially interested in the genomics work Genescient has completed to identify human genes of aging. This knowledge, gained from decades of selective breeding of model animals for longevity, will to lead to the production of nutrigenomic compounds in 2010. The plan is to build on this work and, in later years, to develop drugs aimed at treating age-associated chronic diseases and provide patients with healthy life extension. We are predicting that Genescient will become a leader in its field, with the knowledge that it now has providing it with a significant head start”.”
Damian Crowe, CEO of Genescient, said “The angel investment enables Genescient to further exploit the treasure trove of human genomic targets it currently owns, the goal being to offer better genomic information and superior health-enhancing products to its clients.”
About Genescient Corporation:
Genescient Corporation is a California evolutionary genomics company. Its technology is based on the genomics of model organisms selectively bred for health and longevity over 30 years. This genomic information is combined with whole-genome data, and massive clinical databases to identify, screen and develop benign therapeutic substances for the treatment of the chronic aging-associated diseases including cardiovascular disease, Type II diabetes, and neurodegenerative diseases. Genescient will also provide its clients with genomic information services that address the genes responsible for the complex genomic trait “rate of aging”.
Contact:
Damian Crowe, CEO
Genescient Corporation
+1 949-333-0058 x3305
admin Press ReleasesComments Off on Genescient Chairman to Speak at Singularity Summit 2009
Irvine, CA, August 24, 2009 — Gregory Benford, Chairman of the Board of Genescient Corporation, will speak at the Singularity Summit 09. The Singularity Summit is a gathering of visionaries in business, science, technology, design, and the arts, coming together to explore the rising impact of science and technology on society. This year’s Summit will take place on October 3 and 4 in Manhattan, and marks the first time that the Singularity Summit will be held on the East coast.
Benford will present on Genescient’s revolutionary approach to extended human longevity, with contiguous enhancements of vigor and function. Genescient is a California systems biology company founded on the use of artificial biological selection to cure the diseases of aging. Genescient’s laboratory animals were selectively bred for longevity over 750 generations – the equivalent of 15,000 human years.
The company’s approach addresses the complex genomic networks that underlie aging and aging-associated diseases such as cardiovascular disease, Type II diabetes and neurodegenerative diseases. Benford will discuss some of the company’s latest results and its upcoming products.
The Singularity Summit was founded by Tyler Emerson, Ray Kurzweil and Peter Thiel. Its objective is to to further understanding and discussion about the Singularity concept and the future of human technological progress.
Benford, a well-known scientist, author and innovator, retired from the University of California, Irvine’s Physics department to co-found Genescient. His presentations are scheduled for 10:15 AM and 1:35 PM, Sunday, October 4.
Learn more about The Singularity Summit 2009 here:
http://www.singularitysummit.com/
About Genescient Corporation:
Genescient Corporation is a California systems biology company using advanced information technology to study the genomics of aging and age-associated disease. Genescient applies 21st century genomic technology to identify, screen and develop benign therapeutic substances for the treatment of the chronic diseases of aging including cardiovascular disease, Type II diabetes, and neurodegenerative diseases.
Contact:
Damian Crowe, CEO
Genescient Corporation
+1 949-333-0058 x3305
http://Genescient.com
Genescient study suggests that, when long-term effects are considered, two commonly ingested stimulants are not created equal. The study compares the effects of two stimulants and two sedatives.
Irvine, CA, August 19, 2009 – What long-term effect does your daily cup of “morning Joe” have on your body? In a study just published in PLoS One scientists at Genescient Corporation, a California biotechnology company, sought to answer that question. The study evaluated the long-term health effects of two stimulants — coffee and chocolate — and two sedatives — valproic acid and lithium.
Caffeine is one of the most widely consumed drugs in the world. It is found in coffee, tea, chocolate, colas and, more recently, “high-energy” drinks. A Johns Hopkins University study on caffeine stated that “in North America, 80-90% of adults report regular use of caffeine.” Most consumers of caffeine generally take it to increase their alertness and wakefulness. Genescient scientists sought to determine whether this increased wakefulness is accompanied by enhanced performance, and whether caffeine had any long-term health benefits.
Any lifelong human study is complicated by lifestyle choices, such as exercise and alcohol consumption, or functional demands, such as late-night driving. To avoid the uncertainty introduced by these external factors, Genescient opted to use the well-studied Drosophila melanogaster, the laboratory fruit fly, as its model organism. The tests measured the long-term functional effects of caffeine on both survival and reproductive functions throughout adult life.
When people consume coffee, they generally feel “up” and “ready to go.” But is this effect a subjective illusion? Consider mating; one of the most demanding things that a male Drosophila ever does. It was no surprise to scientists that lithium depressed male mating success; lithium is known to suppress activity. Surprisingly, caffeine also consistently impaired mating success in Genescient’s experiments. By contrast, at normal doses theobromine (the chief stimulant in chocolate) was benign. Worse still, caffeine impaired survival and female reproduction. Again, theobromine proved relatively benign for survival and reproduction.
Lest they be tempted to celebrate, chocolate lovers should be aware that chocolate also contains caffeine. Still, consumption of chocolate should provide the stimulative effects of theobromine without the negative effect of high doses of caffeine. The test results show that the less caffeine the model animals consumed, the better they did.
While Drosophila aren’t people, and the results obtained in model animals may not necessarily carry over to humans, many of the important developmental and metabolic pathways are shared by both species. With this in mind, Genescient’s results suggest that caffeine consumers might want to think twice before drinking that 4th cup of coffee or loading up on energy drinks for that all-night study session.
Genescient Corporation is a California systems biology company using advanced information technology to study the genomics of aging and age-associated disease. Genescient applies 21st century genomic technology to identify, screen and develop benign therapeutic substances for the treatment of the chronic diseases of aging including cardiovascular disease, Type II diabetes, and neurodegenerative diseases. Genescient does not now market, produce, or develop therapeutics containing any of the substances tested in the publication described in this press release.
Contact:
Damian Crowe, CEO
Genescient Corporation
+1 949-333-0058 x3305 http://Genescient.com
Aging is not simply an accumulation of damage or inappropriate higher-order signaling. Aging occurs because of the extensive absence of adaptive genomic information required for survival to later adult ages.
Aging is not simply an accumulation of damage or inappropriate higher-order signaling, though it does secondarily involve both of these subsidiary mechanisms. Rather, aging occurs because of the extensive absence of adaptive genomic information required for survival to, and function at, later adult ages, due to the declining forces of natural selection during adult life.
This absence of information then secondarily leads to misallocations and damage at every level of biological organization. But the primary problem is a failure of adaptation at later ages. Contemporary proposals concerning means by which human aging can be ended or cured which are based on simple signaling or damage theories will thus reliably fail. Strategies based on reverse-engineering age-extended adaptation using experimental evolution and genomics offer the prospect of systematically greater success.
admin News & Features, Press ReleasesComments Off on Genescient and Kronos Announce Alzheimer’s Disease Collaboration
Genescient Corporation and Kronos Science Laboratory will work together to analyze the Kronos Alzheimer’s Case-Control Database, considered to be the finest Alzheimer’s Disease genetic data set in the US. The companies hope to identify genes previously unrecognized genes that are involved in Alzheimer’s Disease.
PET scan of a human brain with Alzheimer’s disease / NIA
Irvine, CA, March 04, 2009 — Genescient Corporation (“Genescient”) and Kronos Science Laboratory, Inc. (“Kronos”) have entered into a collaborative agreement. Genescient will use its proprietary genomic technology to analyze Kronos’ Alzheimer’s Case-Control data set. The companies hope to identify genes that may be involved in Alzheimer’s Disease, but have yet to be recognized. The Kronos Alzheimer’s data is considered to be the highest quality Alzheimer’s Disease genetic data set in the US.
A recent study by Johns Hopkins University estimates that in 2006, Alzheimer’s Disease affected 26.6 million people worldwide. This number is expected to quadruple by 2050. The Alzheimer’s Association estimates that “the direct costs to Medicare and Medicaid for care for people with Alzheimer’s and other dementias and the indirect costs to business for employees who are caregivers of persons with Alzheimer’s and other dementias amount to more than $148 billion annually.”
Genescient has already identified over 750 unique human genomic pathways that may be associated with the diseases of aging; of these, it has verified over one hundred. These pathways are implicated in cardiovascular disease, Diabetes Type II, and other chronic diseases. Genescient will use its knowledge of the pathways it has discovered, to probe the Kronos Alzheimer’s Disease data set.
Genescient’s approach is a marked departure from the standard method of identifying correlation between genes and disease. Whereas conventional approaches seek to identify individual genetic pathways responsible for disease, modern biology has demonstrated that single genetic pathway diseases are the exception. Most diseases, particularly the aging-related diseases that Genescient is concerned with, are caused by complex interactions within genomic networks.
While other approaches see only small parts of the genomic networks responsible for a disease, Genescient’s technology enables researchers to probe the entire biochemical machinery behind chronic diseases. This insight puts Genescient at the leading edge of a revolution in medicine that may ultimately lead to effective treatments for aging, the disorder that ultimately kills most of us.
About Genescient Corporation:
Genescient Corporation is a California genomics company specializing in the discovery and screening of therapeutic substances for the treatment of the chronic diseases of aging.
About Kronos Science Laboratory, Inc.:
Kronos Science Laboratory is dedicated to the discovery and commercialization of innovative new technologies for the improvement of human health and longevity. Kronos also operates the Kronos Longitudinal Aging Study (“KLAS”).
Contact:
Damian Crowe, CEO
Genescient Corporation
+1 949-333-0058 x3305 http://Genescient.com
Evolutionary biology provides the only cogent, formally developed, and experimentally corroborated theory for biological ageing. In this essay, we supply a brisk run through the highlights of evolutionary research on the biology of ageing.
MICHAEL R. ROSE, MOLLY K. BURKE, PARVIN SHAHRESTANI and LAURENCE D. MUELLER
Department of Ecology and Evolutionary Biology, University of California, Irvine, CA 92697-2525, USA
In the late 19th century, the evolutionary approach to the problem of ageing was initiated by August Weismann, who argued that natural selection was more important for ageing than any physiological mechanism. In the mid-twentieth century, J. B. S. Haldane, P. B. Medawar and G. C. Williams informally argued that the force of natural selection falls with adult age.
In 1966, W. D. Hamilton published formal equations that showed mathematically that two ‘forces of natural selection’ do indeed decline with age, though his analysis was not genetically explicit. Brian Charlesworth then developed the required mathematical population genetics for the evolution of ageing in the 1970’s. In the 1980’s, experiments using Drosophila showed that the rate of ageing evolves as predicted by Hamilton’s ‘forces of natural selection’. The discovery of the cessation of ageing late in life in the 1990’s was followed by its explanation in terms of evolutionary theory based on Hamilton’s forces.
Recently, it has been shown that the cessation of ageing can also be manipulated experimentally using Hamilton’s ‘forces of natural selection’. Despite the success of evolutionary research on ageing, mainstream gerontological research has largely ignored both this work and the opportunity that it provides for effective intervention in ageing.
admin Media CoverageComments Off on Live Longer With Evolution? Evidence May Lie in Fruit Flies
Through selective breeding, Dr. Rose was able to create a long-lived line of creatures he called Methuselah flies. He then put his research into reverse and developed flies with much shortened life spans.
A Conversation With Michael R. Rose
By Claudia Dreifus
December 6, 2005
Excerpt from the December 6, 2005 issue of The New York Times (published online December 6, 2005)
Drosophila Melanogaster Photo: michael*
In the 1970’s, Michael R. Rose made scientific history with experiments manipulating the life spans of fruit flies.
Through selective breeding, Dr. Rose was able to create a long-lived line of creatures he called Methuselah flies. He then put his research into reverse and developed flies with much shortened life spans.
All this was accomplished within 12 generations by accelerating the evolutionary processes in a laboratory setting.
These days Dr. Rose, who is 50, breeds fruit flies at the University of California, Irvine, where he is a professor of evolutionary biology. From there, he also directs the Intercampus Research Program on Experimental Evolution for the University of California system . . .
. . . Q. Do you believe there is such a thing as a limited life span for humans?
A. No. Life span is totally tunable. In my lab, we tune it up and down all the time.
And it’s quite clear that the human primate life span got tuned up by evolution over the course of the last few million years.
Almost certainly, we once had the life span of chimpanzees – which is half of what humans have. But we were smarter, able to kill our predators, make deadly tools, find more food, so evolution took us in hand, and we lived longer . . .
Some seriously weird things are springing out of the twisted tangle of our DNA.
by Jerold M. Lowenstein
Excerpt from the December 1992 issue, of Discover Magazine (published online December 1, 1992)
. . . Alternatively, some other newfound oddities, the Methuselah genes, may lengthen the lives of their carriers. The genes (named for the most long-lived man in the Bible) were found in fruit flies by Michael Rose, a geneticist at the University of California at Irvine. Last February, Rose reported that one of these genes makes a souped-up version of superoxide dismutase, an enzyme that mops up highly reactive molecules called free radicals. Like acid rain, these radicals attack and damage any bodily structures they come in contact with. Biologists have suspected for at least two decades that they are largely responsible for the aging process . . .
