65 replies to this topic

[Mind]

Check this forum often throughout the weekend for coverage of the UABBA UCLA conference. I will try to post updates on the presentations as well as conduct interviews through the Ustream channel throughout the weekend.

[Mind]

The first event I will attempt to cover live is the press conference this afternoon. It is coming up in 1 hour (21:00 GMT). I am not sure if there is wireless access. So I might have to write a review after the fact.

[Mind]

Success! I have the Ustream channel up and running for the press conference, which is starting a bit late. It is 20:30 GMT right now. The press conference should be starting in a few minutes. Feel free to ask questions in this forum or at the Ustream channel.

[Mind]

I will be updating this forum as the evening moves along and try to summarize the presentations and questions. No live streaming until most likely - tomorrow. I will try to interview some of the researchers in between presentations.

[Mind]

A partial recording of the UABBA opening press conference is available at the Ustream site. Nothing super special. My laptop crashed near the end. Aubrey, Chui, West, etc... made some statements and answered a few questions.

[Mind]

Unfortunately, I did not see any local news media at the press conference. I thought there would be more in attendance. Perhaps we are in a media town where everyone is more concerned with stardom than with saving their lives. Actually, most of the famous actors and actresses should be very interested in SENS, since it could rejuvenate them and keep their careers alive.

Jason Silva was at the press conference, several bloggers, independent writers, but no local TV as far as I could tell.

[brokenportal]

No media.... Do you think theres a better chance theyll be there tomorrow? Maybe you could call around tonight. I emailed a bunch of media from here but it was hard finding the local contacts.

If you stream a lot more of it do you think the quality would be good enough to be accepted by a health channel somewhere or pbs or something later?

[Mind]

Susan Fonseca Klein opened the conference with thanks to all the sponsors - including the Immortality Institute. I was happy to hear Imminst mentioned at such a large event.

Aubrey was the first speaker and gave an abbreviated version of the SENS speech most of you have seen online. Someone mentioned that many of the presentations will be available online, pending approval of the speakers.

William Haseltine is up now. Making the case that DNA is immortal and we should eventually be able to "attach an individual to the immortality of DNA". Haseltine is speaking about breakthroughs in the last year of stem cell research - changing any cell in your body into a stem cell - and then using those cells to make any type of cell that your body needs AND make it any age that you want it - ie. youthful cells.

Something else I should mention from the press conference. Chui announced that his immuno-cancer therapy is moving into phase 2 trials - pretty quick movement on this treatment. Michael West announced a new effort to catalog all the different cell types within the human body or at least all cells that have been created from stem cells. I can't remember the exact details, but he will be mentioning it later in the weekend as well. It is a new website and collaborative effort. I try to get the name of the site eventually.

[Mind]

Brokenportal. The best I have is my microsoft v6000 webcam, pretty good, but not sure if it will be good enough for the use you mentioned. Also, thanks Eric for all your efforts trying to get media here. You are a SUPER advocate. You need to clone yourself! lol

[Mind]

Haseltine is continuing on talking about all the breakthroughs in modern medicine, genomics, nano, electronic prosthetics. He is covering a lot of stuff that we have discussed here in the forums over the last year. He closed with an optimistic projection that we will be seeing a lot of these therapies (stem cells what not) within the next 10 years! Aubrey cautioned that while most of the people on the panel are optimists, that the therapies might take much longer.

[Mind]

Ames is speaking about Mitochondria function and how it causes aging. He is starting out with some technical slides about how mitos work. He is talking about how Acetyl L-carnitine and Lipoic acid and how they keep mitos younger looking and functioning better.

Now he is moving on to talking about the 40 micronutrients needed to keep your metabolism running properly. He made a good joke about if you are missing one of these nutrients you will die. It was a great dead-pan type joke that made the entire audience laugh. He is making the claim that aging is accelerated if you don't have enough of any one of these micronutrients. He calls this "triage" - where your body shuts down long term metabolic processes in favor of short term reproduction - it stops DNA repair and such things - in favor of just keeping you alive for a couple years longer - long enough to reproduce.

[Mind]

Ames is detailing for the audience how much of the U.S. population is missing their micro nutrients. It is kind-of sad to see how many people do not get simple things like enough iron, magnesium, folate, or even vitamin E. My wife mentioned to me that Ames is scaring her into eating better.

He compared not getting enough folate (which leads to double strand chromosome breaks) to having your cells radiated by large amounts of x-rays.

He spoke about how too much iron is bad as well as too little iron. Most men get too much iron and most women and children do not have enough.

He did research on every micronutrient and how missing each one ages you faster and causes more DNA damage. He also claimed that missing some of these micronutrients leads to a malfunctioning immune system - and will have a paper coming out on this soon.

[Mind]

Michael West (Geron, Advanced Cell, BioTime Inc.) is up now.

He is covering ESCs. Similar to the press conference, he is talking about how having stem cells available (just in the last couple of years) will lead to regenerative medicine. He is very optimistic because ESCs are immortal - they can divide forever.

Now he is moving on to the challenges to implementing ESCs based therapy:

#1 The thousands of different cell types within the human body - enormous complexity. Complex and diverse markers.
#2 purity of stem cells - FDA wants to know if they stem cells someone will be getting are a pure sample - not containing other cells. Regulation issues.
#3 scaling issues (large scale industrial production of stem cell types)

He says he is optimistic because of increasing computer power. We now have the capability to handle all the data generated from the genome project and all the work with stem cells.

Embryome.com is the new OPEN-SOURCE website collaboration West created (or at least advises on) in order to get a handle on all of the complexity involved with ESCs. He is calling on everyone to help out with the Embryome website.

[Mind]

My wife is reviewing the speakers. She thought Ames was the best so far - the most humerous. He also had a lot of information (nutrition) which is applicable and easy to understand.

[Mind]

Aubrey is back up to introduce the second half of the panel. This focus is "why fight aging". He is again talking about advocacy, many ideas/arguments that we (imminsters) are all familiar with.

Why are people against life extension:

#1 Fear of the unknown.
#2 it used to be rational to oppose aging research because the tools/treatments were so complex and hard to imagine - that is not longer so.
#3 "The human cost crushes us". They can't emotionally handle aging and all the things ghastly things that come with it - so they just put it out of their minds.

[Mind]

Gregory Stock is up now.

How do people deal with agiing:

1. ignore it.
2. accept it. "Aging is great". Leon Kass approach.
3. Its impossible.
4. battle it.

He mentioned how the goal of biogerontology today is to compress morbidity, but that is not good enough. He says people who argue for compressed morbidity are not thinking things through enough - we would not really like to fall apart in a matter of months at the end of life - like a salmon. He argues we should battle aging - we should create a war on aging - because it is not a disease but "the disease".

"Can we justify spending the money on aging remedies?" Stock of course argues yes - and with public funds - like a Manhattan project.

1. Aging interventions would be very valuable and desired among a wide section of society - individual benefits.
2. Broad society-level benefits. Should be obvious. Society expends a lot of effort raising and educating young humans - and once they reach maturity then aging starts to take away their functionality - thus wasting the effort.
3. Huge monetary benefit. Aging remedies would help out medicare, health care burdens, social security, etc...
4. It is consistent with all other health programs such as vaccinations, disease prevention.

[Mind]

Picture of Gregory Stock Presenting.

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[Mind]

Bernard Siegel now presenting. He is a lawyer by trade but now is interested in aging research.

He founded the Genetics Policy Institute.

He was involved in the sham case of the first cloned baby that the Raeliens claimed to have produced. Clonaid/Raelians were the only people being quoted on human cloning at the time. Scientists thanked Siegel for debunking Clonaid.

Siegel likens the aging debate and public funding to the abortion debate. He says funding is reduced - in part - do to religious objection. He has debated many people regarding the Adult stem cell vs. Embryonic stem cells. He says, the people who object to ESCs say adult stem cells are better because their is no success yet with ESCs. He likens the objections to ESCs to the Catholic inquisition of Galileo. He claims these people are afraid of change.

He discussed the "Brownback Bill". A bill in the U.S. that would put researchers who engaged in therapeutic cloning (not reproductive cloning) in jail for 10 years and fine them 1 million dollars. The bill would also send people to jail who traveled to a foreign country and got a treatment that involved therapeutic cloning.

He encouraged people to join Americans for Cures. He says the effort should not be based on narcissism but on social good. He argues this is the only way we (advocates) will be successful.

Picture of Siegel Presenting:

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[Mind]

Lastly tonight is Daniel Perry: Executive Director of the Alliance for Aging Research.

He started with the fact that #6 on the list of Science magazine's big questions that will be known within the next 25 years is "how long can we extend human lifespan".

He is focusing on "what can our best scientists learn about aging processes and how can we use it to our advantage". Pretty simple question, but hard to get people and politicians interested. Perry says Biogerontology has the most to "give" to society yet has the least funding and the least interest.

He notified the audience of a paper coming out in a few weeks - by leading international and U.S. biogerontologists - that will argue for a new paradigm in aging research - including slowing aging.

He says one big hurdle is that longevity science has an "image problem". People have been searching for 100s of years for the "fountain of youth" yet have never been successful. He says today it is different because of all the new information and tools we have at our disposal. He argues we need public funding and backing from national policy makers.

He says most politicians do not understand science and medicine well enough to promote longevity science. They will not stick their neck out for fear of losing the next election. He says many scientists do not think about or promote aging research because they are focused on particular diseases - not aging as a whole. Also, most lay people just don't think it is possible (a theme other presenters mentioned).

How do we convince people:

#1 political leaders need to know what is coming our way - trillions of dollars of health care spending - most of which is spent on aging related diseases of the elderly. By 2030 Alzheimer's disease alone will cost 1 trillion dollars alone.

#2 need to get mainstream biogerontologists to support longevity science.

#3. Need credible and statistically valid data that shows success turning back the aging clock - even if it is in a mouse model.

Perry would like to put together a white paper that clearly shows longevity science would offer a tremendous economic benefit to society. He also would like to change the paradigm of attacking aging just one disease at a time.

[Mind]

I would estimate there are about 400 people in attendance - but maybe as many as 600. A good turn-out I think. Everyone is engaged.

[Mind]

Questions now. One person asked about pesticides and cell phones and other dangers. Ames said threats from these things are very tiny and hard to measure.

During the talks it did look like a couple local news stations showed up to get video.

Attached Files

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[Mind]

Aubrey introduced the session this morning and made a statement about videotaping the speakers. He said the Methuselah Foundation will attempt to make many videos available after the conference, but they don't have release forms yet, so it might be awhile.

Adam Arkin is speaking first: "How characterization and creation are creating a new biological engineering science".

The gist of his presentation is that synthetic biology is just like engineering computer chips. Biologists just need to describe all of the modules that evolution has provided. He suggest new "smart drugs" will be and should be manufactured/designed bacteria.

He used AIDS as an example - mentioning a new treatment that uses a modified HIV virus to compete with the deadly version. It uses the same reproduction cycle as "wild" HIV and infects CD4 T cells. Having the modified HIV present in the same space as wild HIV reduces the effects of wild HIV. This is an early example of the type of new synthetic biology Arkin expects future.

Aside: One interesting point he made is that researchers still are not sure how HIV causes AIDS - it is a contentious debate. He also mentioned that some people get infected with HIV but never get AIDS.

http://parts.mit.edu - a website collaboration cataloging different parts/modules of bacteria.

[Mind]

Jan Vijg: "Stochastic mechanisms of gene deregulation in aging"

Vijg showed how DNA mutations/damage accumulate throughout life (point mutations and genome rearrangements). The damage causes genetic and epigenetic drift within tissues. The damage does not affect the individual cells as much as it affects the tissues as a whole. In late-life, tissues within the body are no longer homogeneous but are a mosaic of cells with different gene regulation and expression. All of this variation with the tissue causes aging (according to Vijg) and this is a very difficult problem to correct.

Mouse aging is associated with increased gene transcriptional noise. He suggests aging needs to be studied at the level of the individual cell (something that many people here agree with)

One thing that popped into my head while listening to this talk was that a person should save a sample of their blood when they are young or maybe even samples of different tissues, because later in life you have a lot of epigenetic changes that may be pathogenic. It makes me wonder if stem cells suffer the same rate of point mutations and genome rearrangements as somatic cells. If so, then will they not be as useful later in life? If you use adult stem cells to replenish/replace your organs/tissues will you end up replicating pathogenic mutations?

[Mind]

Jerry Shay: "Telomerase-immortalized cells have stem cell characteristics"

He started with some data of how shortening telomeres correlate highly with many chronic human diseases and pathologies. Most pre-malignant tissues have very short telomeres. Over 90% of human cancer tissue over-express telomerase.

He focused on one particular disease - IPF - Idiopathic Pulmonary Fibrosis. Diseases such as IPF suggest that a full human lifespan requires adequate/sufficient telomerase activity. He mentioned that telomerase is a jekyl and hyde scenario. Many cancer researchers try to shut down telomerase, but for regenerative medicine telomerase may be a key to keeping cells viable.

Mutations in components of the telomerase complex may lead to premature stem cell depletion.

He listed all of the different cells that his lab has "immortalized". He gave an example of skin cells. The immortalized skin cells behaved like normal skin cells and were not cancerous (telomerase did not make the skin cells cancerous). He showed the same results for corneal cells. He believes that telomerase introduction will be very beneficial for tissue engineering.

He cautioned that telomerase activity is only a small part of the aging process/problem.

[Athanasios]

Great stuff, Mind. Thanks for posting these updates.

This, below, makes me think of increased, or non-declining, DNA repair and possible alleviation of mtDNA mutation via autophagy in calorie restriction.

Jan Vijg: "Stochastic mechanisms of gene deregulation in aging"

Vijg showed how DNA mutations/damage accumulate throughout life (point mutations and genome rearrangements). The damage causes genetic and epigenetic drift within tissues. The damage does not affect the individual cells as much as it affects the tissues as a whole. In late-life, tissues within the body are no longer homogeneous but are a mosaic of cells with different gene regulation and expression. All of this variation with the tissue causes aging (according to Vijg) and this is a very difficult problem to correct.

[Mind]

Laura Briggs: "The struggle to keep our telomeres long".

Solutions for life extension (involving telomerase)

1. WILT (SENS approach)
2. Cure cancer first, then activate hTERT and ALT (turn-on telomerase)

Her company has been searching for compounds that will activate telomerase. They have analyzed over 300,000 compounds in the last 9 years. She focused on one particular compound (unnamed) that showed telomerase activation. She showed that this new compound (#57684) was in some cases 20 times more potent in activating telomerase than TA-65 (from TA Sciences). One downside of #57684 is that it is mildly cytotoxic. Her company (Sierra Sciences) is now investigating if 57684 causes DNA damage. One big problem with 57684 is that it affects many different genes (a couple thousand at least) whereas TA-65 only upregulates 32.

This was a highly specialized presentation that focused on one particular compound in one area of longevity science (telomerase activation).

I like Sierra Sciences' tagline "Cure Aging or Die Trying".

[Mind]

Great stuff, Mind. Thanks for posting these updates.

This, below, makes me think of increased, or non-declining, DNA repair and possible alleviation of mtDNA mutation via autophagy in calorie restriction.

Jan Vijg: "Stochastic mechanisms of gene deregulation in aging"

Vijg showed how DNA mutations/damage accumulate throughout life (point mutations and genome rearrangements). The damage causes genetic and epigenetic drift within tissues. The damage does not affect the individual cells as much as it affects the tissues as a whole. In late-life, tissues within the body are no longer homogeneous but are a mosaic of cells with different gene regulation and expression. All of this variation with the tissue causes aging (according to Vijg) and this is a very difficult problem to correct.

So you are suggesting that autophagy is a key mechanism for preventing genetic and epigenetic drift and lessen the pathogenic effects later in life, and that CR may increase lifespan through this mechanism (increased or more efficient autophagy)? CR of course has many other beneficial effects, but this one could be very important.

[Mind]

Claudia Gravekamp: "Improvement of cancer vaccination at older age".

Gravekamp's abstract mentioned an important point (that I have mentioned many times in the past): Your age is the important risk factor for cancer. Recently I read, can't remember where, that your risk of cancer increases up until age 65 and then it levels off - anyone have a reference?

Claudia mentioned that many cancer therapies are effective against primary tumors but not against metastasis. Vaccination is much more effective against metastasis.

The gist of this presentation is that cancer vaccination (programming your immune system to devour cancer) is much more effective at a young age (mouse models) than at an old age. (my assessment: Now it appears that not only does old age correlate highly with cancer incidence but also with the effectiveness of cancer vaccines. a double whammy)

Gravekamp is investigating ways to increase cancer vaccination efficacy in older age (after all that is where it will be most important because most cancer patients are older aged)

c-di-GMP is a small molecule that activates innate and adaptive immune response and might help with cancer vaccination
She also described using Listeria to infect tumor cells and kill them. It is apparently very effective in mouse models, however, I wasn't able to get a lot of the details on how this works - computer crash - darn Vista. During the question period Gravekamp stated she didn't know exactly how Listeria kills tumor cells but that it probably has to do with the mitochondria of the tumor cells.

[Mind]

Next up and highly anticipated is Zheng Cui: "Natural Cancer Resistance in Mice and in Humans: basis for a novel cancer therapy.

Cui provided a new website describing a phase 2 clinical trial based on his therapy: www1.wfubmc.edu/lift

The theory of natural cancer resistance is fairly old - at least 50 years - however no one was able to prove it.

The cancer-resistant mouse originally discovered in Cui's lab was able to pass on its cancer resistance. It is an immunologic process. (details here: http://www1.wfubmc.edu/LIFT/study/)

He showed an amazing video of immune cells (mouse models) forming "rosettes" around cancer cells. The immune cells surround the cancer cells and destroy them. He showed a video he called the "smart bomb". It was a single white blood cell coming into contact with a cancer cell and "popping it" - killing it extremely quickly. I briefly looked at his website but did not see the videos.

He showed a slide indicating a correlation between seasonal changes and cancer incidence. It appears that people who live near the equator (no seasonal change) have a lower incidence in cancer. Cui suggests that this has to do with the fact that immune response declines with the seasons. People who live farther from the equator have weaker immune response during the winter and thus are more susceptible to cancer.

He closed with his therapy's affect on prostate cancer. There was a researcher who challenged him to cure prostate cancer with his immune therapy. This fellow said he would believe Cui if his therapy cured prostate cancer. Cui's therapy was 100% effective against prostate cancer! (not sure in vitro/in vivo experiment) Wow!

[Athanasios]

So you are suggesting that autophagy is a key mechanism for preventing genetic and epigenetic drift and lessen the pathogenic effects later in life, and that CR may increase lifespan through this mechanism (increased or more efficient autophagy)? CR of course has many other beneficial effects, but this one could be very important.

The macroautophagy is thought to keep the numbers of leaky mitochondria down and help preserve mtDNA and organelles. CR increases DNA repair but also is thought to prevent damage as well. I was thinking that some of the genetic expression changes that happen with CR looks to be important and may prevent or alleviate the 'mosaic of cells with different gene regulation and expression'.

See: http://www.pnas.org/...a9214686582acfb

We have presented three previously undescribed results. First, CR begun relatively late in the lifespan of mice was as effective as CR begun early in life at decelerating mortality rate, extending remaining lifespan, and delaying the onset and/or progression of cancer as a cause of death. Second, CR appeared to act rapidly to induce these benefits. The deceleration of aging and reduction in cancer mortality began after 2 months of CR. These results suggest that CR may be more proactive in its effects than previously thought. Finally, the initiation of the health and longevity effects of CR coincided with the induction of 72% of the LT-CR-related genomic profile. Ninety percent of the effects of LT-CR were rapidly reversed by control feeding. Thus, the rapid genomic effects of CR may be causally linked to its beneficial physiological effects. These results increase the likelihood that therapies mimicking the rapid gene expression biomarkers of CR will be effective at inducing its beneficial physiological effects.

and: http://cardiovascres...d6a577b36a20eb2

Heart and skeletal muscle undergo major age-related alterations in gene expression. Gene expression patterns suggest induction of stress response pathways and reduced expression of genes involved in energy metabolism, both of which are broadly prevented by long-term CR in rodents...Because the pathophysiology of aging is complex, it is likely that a detailed analysis of gene expression profiles in multiple tissues will reveal both tissue-specific and general patterns. However, certain limitations remain associated with data generated by microarrays. First, the observed collection of gene expression alterations in whole tissues such as muscle and heart is complex, reflecting the presence of diverse cell types. Secondly, changes in mRNA levels may not always result in a parallel alteration in protein levels. Moreover, changes in mRNA levels may be due to age-dependent changes in mRNA decay processes, such as the reported decline of mRNA stabilizing protein ARE-HuR with aging [65]. However, the complete or partial prevention of the majority of the observed aging alterations by CR in heart and skeletal muscle suggests that gene expression patterns can be used to assess the biological age of the tissue under study, and to infer mechanisms of action of CR 9. Gene expression profiling may also prove valuable to a new area in CR research, the discovery of nutrient or drug interventions that mimic the calorie-restricted state