"The Aging Revolution - - Longevity in the 21st Century: Mitochondrial Peptides and Aging
Research at USC"
Pinchas Cohen, M.D., Dean, USC Davis School of Gerontology
Executive Director, Ethel Percy Andrus Gerontology Center
William and Sylvia Kugel Dean's Chair in Gerontology
Office Location: GER 103
Davis School of Gerontology
University of Southern California
3715 McClintock Avenue
Los Angeles, CA 90089-0191
Office Phone: 213-740-1354
Dr. Cohen's research on aging, neurodegeneration, cancer, and diabetes includes the emerging science of mitochondrial-derived peptides (which he co-discovered), specifically humanin, a 24 amino-acid peptide encoded from the mt-16S-rRNA; this is a novel, centrally- acting, insulin sensitizer, and metaboloprotective factor representing a new therapeutic and diagnostic target in Diabetes and related diseases.
Dr. Cohen held his first faculty position at the University of Pennsylvania from 1992 to 1999. Up to summer 2012, he was a Professor and Vice Chair for Research at the Mattel Children's Hospital at UCLA, as well as the Co-Director of the UCSD/UCLA Diabetes Research Center. He received numerous awards for his research, including a National Institute of Aging "EUREKA"-Award and the NIH-Director-Transformative RO1-Grant. He also recently received the Glenn Award for Research in Biological Mechanisms of Aging.
He holds several patents for novel peptides and is the Co-Founder of CohBar, a biotechnology company developing mitochondrial peptides for diabetes. Dr. Cohen has published over 250 papers in top scientific journals focusing on aging, Alzheimer's Disease, cancer, Diabetes, Growth Hormone, IGF-biology, and the emerging science of mitochondrial-derived peptides, which he discovered specifically, humanin, a 24 amino-acid peptide encoded from the mt-16S-rRNA. It is a novel, centrally acting, insulin sensitizer and metaboloprotective factor representing a new therapeutic and diagnostic target in diabetes and related disease.
Dr. Cohen is President-elect of the Growth Hormone Society and served on the Endocrine Society Steering Committee. He sits on multiple NIH study sections and on several editorial boards.
Dr. Cohen is leading several new initiatives at the USC Davis School, including the development of a center for digital aging, and a major focus on the creation of tools for "personalized aging," an approach he has been spearheading for the purpose of garnering the latest technologies such as genomics towards individualizing healthy aging strategies, that has been featured in the Milken Global Conference and in the Bloomberg Longevity Economy Conference.
M.D., Faculty of Medicine, Technion, Haifa, ISRAEL, 1986
Postdoctoral training, Stanford University [1986 - 1992]
1. Milman S, Atzmon G, Huffman DM, Wan J, Crandall JP, Cohen P, and Barzilai N., "Low Insulin-Like Growth Factor-1 Level Predicts Survival in Humans with Exceptional Longevity," Aging Cell. 2014 March 12. doi: 10.1111/acel.12213. [E-pub ahead of print] PMID: 24618355.
2. Levine ME, Suarez JA, Brandhorst S, Balasubramanian P, Cheng CW, Madia F, Fontana L, Mirisola MG, Guevara-Aguirre J, Wan J, Passarino G, Kennedy BK, Wei M, Cohen P, Crimmins EM, and Longo VD.,"Low Protein Intake Is Associated with a Major Reduction in IGF-1, Cancer, and Overall Mortality in the 65 and Younger, But Not Older Population," Cell Metab. 2014 March 4; 19(3), pp. 407-17. doi: 10.1016/j.cmet.2014.02.006. PMID: 24606898 [in process]
3. P. Cohen, "New Role for the Mitochondrial Peptide Humanin: Protective Agent against Chemotherapy-Induced Side Effects," Journal of the Natl. Cancer Inst. 2014 Mar 1; 106(3):dju006. doi: 10.1093/jnci/dju006. Epub 2014 Mar 1. No abstract available.
April 28, 2014; 8:00 PM
"CNN-TV Documentary: How To Live Forever"
For tonight's meeting we will play the one-hour CNN-TV documentary hosted by Morgan Spurlock "Inside Man: How To Live Forever" first shown on Sunday, April 13, 2014; 10:00 PM PDT.
In "Futurism," an episode in CNN's original series, "Morgan Spurlock: Inside Man" on Sunday, April 20th (10:00 PM EDT/PDT), Spurlock enters the "brave new world of extreme life extension. He embarks on a life-prolonging regimen and tries everything from lifestyle habits, to genome hacking, to creating an avatar and uploading his consciousness in preparation for the 'Technological Singularity.' Spurlock's quest to live forever includes visits with the Maximum Life Foundation, radical futurist Ray Kurzweil, Stanford University's Virtual Human Interaction Lab, Cambrian Genomics in San Francisco, North Carolina's Wake Forest Institute for Regenerative Medicine, and Denver's Grossman Wellness Center in Golden, CO.
March 10, 2014; 8:00 PM
"Aging, Protein Aggregation, and Neurodegeneraton: On the Paradoxical Effect of TTR
(Transthyretin) on Neurons and Alzheimer's Disease"
Prof. Joel N. Buxbaum, M.D.
Keck Autoimmune Disease Center
Department of Molecular and Experimental Medicine
The Scripps Research Institute
10550 North Torrey Pines Road
La Jolla, CA 92037
Prof. Joel N. Buxbaum, M.D. is a Pathologist from the Scrips in San Diego, who has researched TTR Amyloidosis for many decades. This talk was given on a Thursday afternoon at 4:00 PM October 24, 2013 as part of our Thursday Weekly Seminar Series for the Molecular Biology Institute in Boyer Hall, Rooms 159/173, hosted this week by L. Stephen Coles, M.D.
1. Buxbaum, Joel N., Ye A., Reixach N., Friske L., Levy C., Das P., Golde T., Masliah E., Roberts, A. R., and Bargtai T., "Transthyretin Protects Alzheimer's Disease Mice from the Behavioral and Biochemical Effects of A-Beta Toxicity," Proc. of the National Academy of Sciences USA; Vol. 105, No. 7, pp. 2681-6 (February 12, 2008) Epub PMID: 18272491.
2. Li, ZX, Masliah E., Rieixach N., Buxbarum, Joel N., "The Systemic Amyloid Precursor Transthyretin InhibitsAlzhimer Neruotodxicity in vivo and in Tissue Culture," Journal of Neuroscience, Vol. 310, pp. 12483-90 (2011) PMID: PMC31272869.
Date: Monday, March 10, 2014
February 10, 2014; 8:00 PM
"Using Epigenetics To Calculate Chronological Age"
Steve Horvath, Ph.D., Professor of Human Genetics and Biostatistics
Department of Biostatistics
UCLA School of Public Health
Los Angeles, CA 90095-1772
Office: 4357A Gonda and 21-254A CHS
Everyone grows older, but scientists don't really understand why. Now a UCLA study has uncovered a biological clock embedded in our genomes that may shed light on why our bodies age and how we can slow the process. Published in the October 21st Edition of Genome Biology, the findings could offer valuable insights into cancer and stem-cell research.
While earlier clocks have been linked to saliva, hormones, and telomeres, the new research is the first to identify an internal timepiece able to accurately gauge the age of diverse human organs, tissues and cell types. Unexpectedly, the clock also found that some parts of the anatomy, like a woman's breast tissue, age faster than the rest of the body.
"To fight aging, we first need an objective way of measuring it. Pinpointing a set of biomarkers that keeps time throughout the body has been a four-year challenge," explained Steve Horvath, a Professor of Human Genetics at the David Geffen School of Medicine at UCLA and of Biostatistics at the UCLA Fielding School of Public Health. "My goal in inventing this clock is to help scientists improve their understanding of what speeds up and slows down the human- aging process."
To create the clock, Horvath focused on methylation, a naturally occurring process that chemically alters DNA. Horvath sifted through 121 sets of data collected previously by researchers who had studied methylation in both healthy and cancerous human tissue.
Gleaning information from nearly 8,000 samples of 51 types of tissue and cells taken from throughout the body, Horvath charted how age affects DNA methylation levels from pre-birth through 101 years. To create the clock, he zeroed in on 353 markers that change with age and are present throughout the body. Horvath tested the clock's effectiveness by comparing a tissue's biological age to its chronological age. When the clock repeatedly proved accurate, he was thrilled - - and a little stunned. "It's surprising that one could develop a clock that reliably keeps time across the human anatomy," he admitted. "My approach really compared apples and oranges, or in this case, very different parts of the body: the brain, heart, lungs, liver, kidney and cartilage."
While most samples' biological ages matched their chronological ages, others diverged significantly. For example, Horvath discovered that a woman's breast tissue ages faster than the rest of her body. "Healthy breast tissue is about two to three years older than the rest of a woman's body," said Horvath. "If a woman has breast cancer, the healthy tissue next to the tumor is an average of 12 years older than the rest of her body." The results may explain why breast cancer is the most common cancer in women. Given that the clock ranked tumor tissue an average of 36 years older than healthy tissue, it could also explain why age is a major risk factor for many cancers in both genders.
Horvath next looked at pluripotent stem cells, adult cells that have been reprogrammed to an embryonic stem-cell-like state, enabling them to forrm any type of cell in the body and continue dividing indefinitely. "My research shows that all stem cells are newborns," he said. "More importantly, the process of transforming a person's cells into pluripotent stem cells resets the cells' clock to zero." In principle, the discovery proves that scientists can rewind the body's biological clock and restore it to zero.
"The big question is whether the biological clock controls a process that leads to aging," Horvath said. "If so, the clock will become an important biomarker for studying new therapeutic approaches to keeping us young."
Finally, Horvath discovered that the clock's rate speeds up or slows down depending on a person's age. "The clock's ticking rate isn't constant," he explained. "It ticks much faster when we're born and growing from children into teenagers, then slows to a constant rate when we reach 20."
In an unexpected finding, the cells of children with Progeria [HGPS], a genetic disorder that causes premature aging, appeared normal and reflected their true chronological age.
UCLA has filed a provisional patent on Horvath's clock. His next studies will examine whether stopping the body's aging clock halts the aging process -or increases cancer risk. He'll also explore whether a similar clock exists in mice.
Brief Biographical Sketch:
B.S. Mathematics and Physics (1989) Technical University of Berlin
Ph.D. in Mathematics (1995) University of North Carolina, Chapel Hill, NC
Doctor of Science in Biostatistics (2000) Harvard School of Public Health
Research and Interests:
Dr. Horvath is a Professor in Human Genetics and Biostatistics at UCLA. His methodological research area lies at the intersection of biostatistics, bioinformatics, computational biology, cancer research, genetics, epidemiology, machine learning, and systems biology. His group applies these methods to study a broad spectrum of diseases, e.g., aging research, cancer, cardiovascular disease, HIV, Huntington's Disease, and Neurodegenerative Diseases.
Systems Biology and Systems Genetics: His group develops and applies methods for
analyzing and integrating gene expression-, DNA methylation-, microRNA, genetic markers-,
and complex phenotype data. In particular, we developed weighted correlation network analysis
(also known as weighted gene co-expression network analysis WGCNA), which is a systems-
biologic data analysis method for analyzing high dimensional "-omics" data. These methods also
lend themselves for comparing different species at the genomic level. A lot of material including
articles, R software tutorials, and youtube lectures can be found here...
Biomarker development: His group works on all aspects of biomarker development: data collection, novel data analysis methods, and biomarker validation studies. For example, they worked on genomic biomarkers of aging and age-related diseases including cancer. We compared standard meta-analysis methods with network-based meta-analysis methods.Machine learning methods: We work both on supervised and unsupervised machine learning methods. For example, we developed the random generalized linear model (randomGLM) predictor, see http://labs.genetics.ucla.edu/horvath/htdocs/RGLM/ random forest clustering (http://labs.genetics.ucla.edu/horvath/RFclustering/RFclustering.htm), and the cluster and propensity based approximation of a network (CPBA).
Genome wide association studies: He has long standing interest in developing and applying allelic association tests, e.g.. he has worked on the Family Based Association Test (FBAT). More recently his group is interested in enhancing GWAS studies and exome sequencing methods.
Epigenomics: Methods and applications surrounding epigenetic data (in particular DNA methylation data) to study human diseases (e.g., age-related diseases). Epigenetics is the study of changes in gene expression or cellular phenotype, caused by mechanisms other than changes in the underlying DNA sequence.
Ref.: Steve Horvath, "DNA Methylation - -Age of Human Tissues and Cell Types," Genome Biology, Vol. 14, No. 10, pp. R115 (2013). PMID: 24138928.
Date: Monday, February 10, 2014
May 12, 2014; Prof. Pinchas Cohen, M.D. Dean of the Davis School of Gerontology at USC.
Canceled: Liana Apostolova, M.D.,
Associate Professor-In-Residence in Neurology Mary S. Easton Center for Alzheimer's Disease Research
10911 Weyburn Avenue, 2nd Floor
Los Angeles, CA 90095-7226
E-mail: "A HREF= "mailto:firstname.lastname@example.org"> apostolpova@mednet. ucla.edu
URL: A HFEF="http://www.adc.ucla.edu"> adc.ucla.edu.
"Alzheimer's Disease: Amyloid Beta and Beyond, Obtaining Clues from Imaging and Genetics."
due to family obligations.
Monday, January 13, 2013; 8:00 PM
"Traumatic Brain Injury: Hormonal Dysfunction"
Clinical Prof. Mark L. Gordon, M.D.
Department of Family Medicine
USC Keck School of Medicine
Los Angeles, California
16661 Ventura Blvd, Suite 716
Encino, CA 91436-1884
According to the CDC there are over 1.9 million cases of non-combatant Traumatic Brain
Injury (TBI) a year. Of that number 53,000 individuals die on the spot, 360,000 end up in a
hospital, and nearly 1.5 million deal with the injury at home never knowing that there is a
potential time-bomb ticking inside their heads.
Unique to mild, moderate, and severe head injuries is the unforeseen development of hormone deficiencies causing the stealth syndrome. This is precipitated by the interruption of hormonal homeostatic mechanisms found within the hypothalamic center of the brain. It is this area that controls the master gland - - The Pituitary. Under stimulation of the pituitary secondary hormones are produces that directly or indirectly stimulate other hormones to be produced by peripheral glands found throughout our body - thyroid, ovaries, testicles, and adrenal glands.
Traumatic Brain Injury is finally being recognized as a causative factor for accelerated hormonal deficiencies. This can cause psychological, physiological, and physical manifestations such as: depression, anxiety, mood swings, memory loss, inability to concentrate, learning disabilities, sleep deprivation, increased risk for heart attacks, strokes, high blood pressure, diabetes, loss of libido, menstrual irregularities, pre-mature menopause, obesity, loss of lean body mass, muscular weakness, and a number of other medically documented conditions.
Studies have shown us that the use of conventional medications (antidepressants, antianxiety, antiseizure, and antipsychotic) do not improve upon the underlying cause creating the symptoms associated with Traumatic Brain Injury (Post-Concussion Syndrome) because they do nothing to increase the missing hormones. Psychotherapy does nothing to increase deficient hormones; it only encourages you to accept a poor quality-of-life and to move on.
Replacement and supplementation with phytohormones and selected natural products can improve upon many of the patient's symptoms. We know this as a fact having started clinical application of the science behind our protocols since 2006. tbimedlegal.com.
The goal of this talk is to provide you with...
(1) An understanding of the means by which all forms of neurotrauma (mild, moderate, and severe) can lead to dysfunction of the hypothalamic/pituitary mechanism of hormonal homeostasis;
(2) Optimal utilization of laboratory testing to monitor the onset and progression of traumatic brain injury related hormonal dysfunction;
(3) Selection of neuroradiology studies to identify areas of damage;
(4) To design and implement a strategy of hormonal intervention and replenishment;
(5) Selection of natural supplements; and
(6) The use of select anti-oxidants for the secondary wave of neurotrauma.
Dr. Gordon is the Medical Director of
Millennium Health Centers, Inc.
Access Med Labs
International Medical Director,
Reignwood Wellness and Trinity Wellness
QSM Scientific, "Enhancing the Science of Delivery"
Medical Consultant, NFL Retiree Committee
Clinical Application of Interventional Endocrinology (2007).
TBI A Clinical Approach to Diagnosis and Treatment (2014).
The Laboratory of Interventional Endocrinology (2014).
Monday, December 9, 2013; 8:00 PM
"A Summary of the Paul Glenn Foundation Conference on Aging at Harvard Medical School on
James P. Watson, M.D.
Dr. James P. Watson, M.D., will give us a report on the 2013 Paul Glenn Conference on Aging (at Harvard Medical School) held on June 17, 2013. Dr. Watson will discuss the talks given by the speakers, their topics, hypotheses, data, conclusions, references, and his own comments.
Eight of the presenters at this one-day meeting were as follows:
1. Bruce Yanker (Harvard; Boston, MA)
2. Thomas Prolla (University of Wisconsin; Madison, WI)
3. Yousin Sun (Albert Einstein College of Medicine; Bronx, NY)
4. Martin Hetzer (Salk Institute; La Jolla, CA)
5. Amy Wagers (Harvard; Boston, MA)
6. Angelika Amon (MIT; Cambridge, MA)
7. Irina Conboy (UC Berkeley; Berkeley, CA)
8. Tom Johnson (University of Colorado; Boulder, CO)
Monday, Veterans Day, November 11, 2013; 8:00 PM
"Lengthening Telomeres to Lengthen Healthspan"
Harvey S. Bartnof, M.D.
University of California at San Francisco
Brief Biographical Sketch:
Dr. Bartnof is the Founder and Medical Director of California Longevity and Vitality
Medical Institute in San Francisco, California.
Raised in Los Angeles, CA, he completed his undergraduate BA (1974) degree with high honors in Biology from the University Of California at San Diego (UCSD) in La Jolla, CA. Dr. Harvey S. Bartnof received his M.D. from the University of California at San Francisco School of Medicine (1978) with honors in Internal Medicine, Pediatrics, Cardiology, Clinical Pharmacology and Otolaryngology. His post-graduate training in Internal Medicine was at Harbor-UCLA Medical Center in Torrance, CA.
Subsequently, he was a full-time Staff Physician at Santa Teresa Community Medical Center in San Jose, CA in Emergency Medicine for eight years [1980 - 1988], followed by more than ten years in Internal Medicine/Family Medicine (Urgent Care, [1988 - 1999]).
Dr. Bartnof was on the clinical faculty in the Department of Medicine at University of California at San Francisco for eight years [1986 - 1993], where he was Course Co-Director of "AIDS-HIV: Overview and Update" and Medical School Training Coordinator for the AIDS Professional Education Project [1987 - 1990]. He also served as Chief Physician at AIDS Virus Education and Research Institute in San Francisco [1985 - 2002] and Medical Editor of www.HIVandHepatitis.com [1998 - 2000]. Dr. Bartnof also served on the Scientific Advisory Committee at the San Francisco AIDS Foundation [1987 - 2001], where he was Chairman [1987 - 1989] and a member of the Board of Directors [1987 - 1989].
Date: Monday, November 11, 2013
So full attention can be given to creating a quality video recording that will be made available on-line, this meeting will not be webcast.
"Extracellular RNA in Saliva"
Prof. David Wong, D.D.S.
Associate Dean for Research and Professor/Director
UCLA Department of Dentistry and Oral Biology and Med/DRI
P. O. Box 951668
Los Angeles, CA 90095-1668
UCLA's School of Dentistry has just received a $5 million grant to study extracellular RNA
in saliva. This research could yield a new method for detecting stomach cancer and other
diseases, like Sjögren's Syndrome, an autoimmune disease that afflicts females over males
by a ratio of 10:1.
We will then discuss a novel theory of molecular signaling by extracellular RNA in saliva.
First, Exosomes (small double-walled lipid-membrane bubbles) may serve as transport vesicles for exotic RNA molecules (miRNA, siRNA [RNAi], shRNA [short hairpin], circRNA, etc.) capable of acrossing extracellular spaces, including saliva and other bodily fluids [like blood and urine], that command adjacent cells to become aligned with a new function (or a larger agenda in response to say, environmental stress). [BTW, saliva is swallowed continuously at the rate of a liter or more per day.]
Secondly, exosomes in the saliva (which are mostly swallowed and not spit out) may even pass through the stomach without being digested by stomach acid and enter the blood stream and/or the lymphatic system (depending on surface proteins) by way of the small intestine, as a back door to orchestrating systemic signaling for many of the distant cells in our body to keep them all functionally synchronized.
Date: Monday, September 9, 2013
"Preliminary Autopsy Results for the Oldest Person in California"
Dr. L. Stephen Coles, M.D., Ph.D., Lecturer in Gerontology
UCLA Molecular Biology Institute
with "Significant Sig" Certificate and Medallion from the Sigma Chi Fraternity, RPI class of 62.
Mrs. Soledad Mexia, 114 yo Hispanic White Female born in Mexico, who lived most of her life in Chula Vista, CA, was the oldest living person in California and the fifth oldest person in the world at the time of her passing. Her anatomical autopsy was performed in the UCLA Pathology and Laboratory Medicine Department in the David Geffen School of Medicine on Friday, August 30th at 1:00 PM PDT. The microscopic and neuropathology portions of the autopsy have yet to be performed. We will keep everyone informed when a final cause-of-death has been established.
Date: Monday, August 5, 2013
Dr. Bryant Villeponteau, Ph.D., Vice President for Research
11180 Warner Avenue, Suite 165
Fountain Valley, CA 92708
The accumulated data from many research groups has shown that aging occurs through
multiple pathways. As the force of natural selection declines with age, selective pressure for
fitness in late-life wanes systematically. I will describe our unpublished work at
Genescient, Inc. on wild-type and Methuselah Drosophila, which provides further
evidence that changes in lifespan involves multiple genetic pathways that become less fit with
age. Using the multi-path concept of aging we have identified critical targets for aging and
substances that act on those gene targets. I will be presenting data on "SC 100" (a multi-targeted
nutritional supplement) that slows aging in Drosophila and doubles their maximum
lifespan. I also show that SC100-treated flies have greatly enhanced resistance to stress
and to A-Beta and Tau-induced dementia.
I am also working with another company (Centagen) to develop the technology to amplify embryonic-like adult stem cells without aging or reducing pluripotent potential.
Lastly, I will discuss my views on our current options with stem cells and the future of longevity research by the year 2030.
Brief Biographical Sketch:
Dr. Villeponteau is President and CSO of Centagen. Inc. of Boulder, CO. He has 30 years of scientific leadership experience and about 60 journal and patent publications. He holds a B.A. in Economics, a M.A. in Biostatistics, and a Ph.D. in Molecular Biology from UCLA. Bryant was Assistant Research Chemist in the Department of Chemistry and Biochemistry at UCLA for four years and Assistant Professor of Biological Chemistry at the University of Michigan Medical School for six years. Bryant then led a research group at Geron Corporation for 4 and 1/2 years, where he was the lead inventor in cloning human telomerase, thereby wining the Distinguished Inventor Award for the 2nd best US patent of 1997. As the Champion of Telomerase Therapeutics at Geron, he also worked on human stem cells, which were pioneered by Geron in the 1990's. Bryant then joined HealthSpan Sciences, Inc. as CSO and later served as CEO for three years. For the next eight years, Dr. Villeponteau served as a VP/Consultant for Sierra Sciences of Reno, NV. From September of 2008 to present, Dr. Villeponteau has been the VP of R&D with Genescient Corporation. Bryant also Co-founded Centagen, incorporated in January of 2009, and Life Code, LLC in October of 2010 in order to market the Stem Cell 100 product line.
Monday, July 8, 2013; 8:00 PM
"Awakened by Cellular Stress: Isolation, Characterization and Clinical Implications of a Novel
Population of Pluripotent Stem Cells Derived from Human Adipose Tissue"
Gregorio D. Chazenbalk, Ph.D., Research Associate
Department of Obstetrics and Gynecology
UCLA David Geffen School of Medicine
Los Angeles, CA 90095-1740
UCLA Scientists have Isolated and Characterized a new population of stress-resistant
pluripotent stem cells in fat tissue removed during liposuction. Researchers from the UCLA
Department of Obstetrics and Gynecology have isolated a new population of primitive,
stress-resistant human pluripotent stem cells easily derived from fat tissue that are able to
differentiate into virtually every cell type in the human body without genetic modification.
The cells, called Multi-lineage Stress-Enduring (Muse-AT) stem cells from fat, or adipose, tissue, were discovered by "scientific accident" when a piece of equipment failed in the lab, killing all the stem cells in the experiment except for the Muse-AT cells. The research team further discovered that not only are Muse-AT cells able to survive severe stress, they may even be activated by it, said study senior author Gregorio Chazenbalk, an Associate Researcher with UCLA Obstetrics and Gynecology.
These pluripotent cells, isolated from fat tissue removed during liposuction, expressed many embryonic stem cell markers and were able to differentiate into muscle, bone, fat, cardiac, neuronal and liver cells. An examination of their genetic characteristics confirmed their specialized functions, as well as their capacity to regenerate tissue when transplanted back into the body following their "awakening."
"This population of cells lies dormant in the fat tissue until it is subjected to very harsh conditions. These cells can survive in conditions in which usually only cancer cells can live," Chazenbalk said. "Upon further investigation and clinical trials, these cells could prove a revolutionary treatment option for numerous diseases, including heart disease, stroke and for tissue damage and neural regeneration."
Purifying and isolating Muse-AT cells does not require the use of a cell sorter or other specialized, high-tech devices. They are able to grow either in suspension, forming cell spheres, or as adherent cells, forming cell aggregates very similar to human embryonic stem cell-derived embryoid bodies.
"We have been able to isolate these cells using a simple and efficient method that takes about six hours from the time the fat tissue is harvested," said Chazenbalk,a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research. "This research offers a new and exciting source of fat stem cells with pluripotent characteristics, as well as a new method for quickly isolating them. These cells also appear to be more primitive than the average fat stem cells, making them potentially superior sources for regenerative medicine."
Currently, embryonic stem cells and induced pluripotent stem cells - - skin cells turned into embryonic-like cells - - are the two main sources of pluripotent cells. However, both types can exhibit an uncontrolled capacity for differentiation and proliferation, leading to the formation of unwanted teratoma, or tumors. "Little progress has been made in resolving that defect," Chazenbalk said.
Muse cells originally were discovered by a research group at Tokohu University in Japan and were derived from bone marrow and skin, rather than fat. That research group showed that Muse cells did not produce teratomas in animal models. Further research on the Muse-AT cells isolated at UCLA will need to be done to determine whether that cell population avoids production of teratomas.
In addition to providing a potential source of cells for regenerative medicine, Chazenbalk said the Muse-AT cells may provide a better understanding of cancer cells, the only other cells known to display such stress resistance.
Going forward, Chazenbalk and his team will use Muse-AT cells in animal models to regenerate damaged or dysfunctional tissue to determine how efficiently they grow and perform in the body and to gauge their potential for future clinical use.
"Because lipoaspiration is a safe and non-invasive procedure and Muse-AT cell isolation requires a simple yet highly efficient purification technique, Muse-AT cells could provide an ideal source of pluripotent-like stem cells," the study states. "Muse-AT cells have the potential to make a critical impact on the field of regenerative medicine."
The study was funded by the UCLA Department of Obstetrics and Gynecology, the Eunice Kennedy Shriver National Institute of Child Health & Human Development , the National Institutes of Health through the cooperative agreement U54 HD071836 and by the Department of Stem Cell Biology at Tohoku University in Japan.
1. Saleh Heneidi, Ariel A. Simerman, Erica Keller, Prapti Singh, Xinmin Li, Daniel A. Dumesic, and Gregorio D. Chazenbalk, "Awakened by Cellular Stress: Isolation and Characterization of a Novel Population of Pluripotent Stem Cells Derived from Human Adipose Tissue" PLoS ONE (June 5, 2013).
2. Health Sciences at UCLA.
Monday, June 10, 2013; 8:00 PM
"Reprogramming Old Human Cells Back to an Embryonic State:"
"Clues to Immortality?"
Clive Svendsen, Ph.D. (Left) leads Dr. Stephen Hawking, third from left, on a tour of the Regenerative Medicine Institute at Cedars-Sinai Medical Center in Los Angeles
(Tuesday, April 9, 2013; AP Photo/Cedars-Sinai, Eric Reed)
Clive Svendsen, Ph.D., Director
Regenerative Medicine Institute
Cedars-Sinai Medical Center
8700 Beverly Blvd, SSB, Room 365
Los Angeles, CA 90048
Phone: 310-248-8072; 310-248-8585
FAX: 310-248-8066; 310-248-8555
I believe reprogramming 100 yo fibroblasts to an embryonic state tells us something quite fundamental about the nature of the aging process. My conclusion is that the more you slow the aging process, the more likely you are to promote the risk of cancer. This will is likely to be our fundamental battle moving forward.
Below is a message from Mr. Johnny Adams regarding how to participate in our web
broadcast for this meeting...
I plan to test and have the webcast running at around 7:30 PM PDT, so feel free to join anytime.
(Tuesday, May 14, 2013 at 3:30 AM GMT in London, UK)
For other locations check the World Time Converter
1. To join, go to www.gotomeeting.com
2. Click "Join a Meeting" It's positioned near the upper right. Color is blue.
3. Enter the meeting ID: 246-265-549
It will ask for your name, and may ask you for your E-mail address. We are paying for this service and to my way of thinking, my E-mail address is none of their business, so I just put in something like email@example.com
We will use the built-in audio conferencing -- not the call in number. This will require computer speakers, and also a microphone if you plan to speak live with other attendees.
Please RSVP to Jadams@AgingInterventionFoundation.org
I will both be transmitting and attending on a separate computer. On-line attendees will be able to talk to one another and send text messages. If I'm not occupied, we'll be able to talk and text messages.
The GotoMeeting setup program asked which countries would have attendees. I clicked all that were available, but many countries were not on the list. I hope that doesn't matter.
I will have my Skype open on the separate attending computer.
Skype ID: AgingIntervention NOT DigitalJohnnyAdams
I will check E-mail as often as possible JAdams@AgingInterventionFoundation.org
Although I don't like to use the GRG list for these kinds of communications, I may send an E-mail to the list during the webcast if anything changes.
Monday, May 13, 2013; 8:00 PM
"Next Generation DNA Sequencing"
Prof. George Church, Ph.D.
Department of Genetics
Harvard Medical School
and Director of personalgenomes.org
The double-helical structure of DNA was deciphered on February 28, 1953 by Drs.
James D. Watson and Francis H. Crick. They immediately appreciated the potential of DNA's
morphology for storing genetic information - - the blueprint of life. For the last 60 years, this
exciting discovery has inspired scientists to decipher the molecule's manifold secrets and resulted
in a steady stream of innovative advances in medical genetics and genomics.
In this webinar by Prof. George Church and colleagues, we examine what the future holds for DNA research, brining together three senior investigators in the field of genetics and genomics.
Original Broadcast Date: Tuesday, March 5, 2013
Click for the Webinar...
Next Generation DNA Sequencing using GoToMeeting.
The advent of Next-Generation Sequencing is considered the most propelling technological
advance, which has resulted in the doubling of sequence data almost every five months and the
precipitous drop in the cost of sequencing a region of DNA. This webinar will track the
evolution of next-generation sequencing and explore what the future holds in terms of the
technology and its medical applications.
1. George Church, Ph.D., Professor, Department of Genetics, Harvard Medical School
2. George Weinstock, Ph.D., Professor of Genetics and Molecular Microbiology, Washington University
3. Joel Dudley, Ph.D., Assistant Professor of Genetics and Genomic Sciences and Director of Biomedical Informatics, Mount Sinai School of Medicine
George Church and Edward Regis, Regenesis: How Sythetic Biology Will Reinvent Nature and Ourselves (Basic Books, New York; 2012).
Monday, April 8, 2013; 8:00 PM
"Brain Activity and Human Consciousness"
L. Stephen Coles, M.D., Ph.D., Lecturer in Gerontology
UCLA Molecular Biology Institute
This lecture briefly covers the topic of human consciousness, including the classic Mind/Body Problem and the problem of Free Will, from the point of view of a neuroscientist. Brain anatomy and neurophysiology are needed to explain what the latest imaging techniques reveal about how the brain works to create sensations, motor functions, thinking, memory, learning, and human language. Finally, we cover a very brief introduction to Clinical Psychology in order to touch on what happens when our brains fail to work properly.
Friday, March 1, 2013; 8:00 PM
"Living to 100 and Beyond: New Discoveries in Longevity Demographics
Do centenarians stop aging? Refutation of 'immortality phase' theory"
Leonid Gavrilov, Ph.D., GSA Fellow
Natalia Gavrilova, Ph.D., GSA Fellow
Center on Aging
NORC at the University of Chicago
Blog: longevity-science blogspot.com
Monday, February 11, 2013; 8:00 PM
Clinic International Conference on Senescent Cells"
Dr. James P. Watson, M.D.
The regular LA-GRG Meeting in January 2013 was canceled due to illness.
Monday, December 10, 2012; 8:00 PM
"The Biology of
Aging Is Now Understood"
Dr. Leonard Hayflick, Ph.D.
Professor of Anatomy
School of Medicine
University of California at San Francisco
The belief that aging is still an unsolved problem in biology is no longer true. To understand this belief, it is necessary to define the four phenomena that characterize the finitude of life: (1) aging; (2) the determinants of longevity; (3) age-associated diseases; and finally (4) death. Age changes can occur in only two fundamental ways: Either (1) as the result of a purposeful program driven by our genes or (2) by stochastic (random) accidental molecular events. These means are not mutually exclusive.
The weight of evidence indicates that a gene-driven program does not govern the aging process itself; what does is the stochastic or random loss of molecular fidelity. Potential longevity is determined by the energetics of molecules present after reproductive maturation, including those that compose the repair machinery involved in turnover, synthesis, and maintenance. The repair and synthesis processes that exceed the appearance of dysfunctional molecules prior to reproductive maturity then shifts so the spread of energy described in The Second Law of Thermodynamics [Entropy] that creates an excess of dysfunctional molecules, begins to exceed their capacity for repair, and the thermodynamic instability characteristic of the aging process begins. The maintenance, repair, and synthetic pathways that maintain the fidelity of molecules produced before and after reproductive maturity determine longevity. Unlike the stochastically-driven aging process, longevity determination is governed by the human genome, our DNA. Furthermore, the aging process is fundamentally distinct from age-associated diseases.
Unlike diseases, changes due to aging occur (a) in every multi-cellular animal that reaches a fixed size in adulthood; (b) cross virtually all species barriers; (c) in all members of a species only after the age of reproductive maturation; (d) in all animals removed from the wild and protected by humans, even when that species probably has not experienced "aging" for thousands or even millions of years; (e) in virtually all animate and inanimate matter; and (f) with the same universal molecular etiology -- that is, thermodynamic instability. Unlike aging, there is no disease or pathology that shares all six properties. Because this critical distinction is rarely understood, the enormous imbalance of resources spent more on studying age-associated disease than conducting research on the fundamental biology of aging cannot be expected to increase our knowledge of the aging process.
Quote: "Studying the longevity of laboratory mice is like studying creatures from Mars."
Brief Biographical Sketch:
Dr. Leonard Hayflick is a Professor of Anatomy at the University of California, San Francisco, School of Medicine, and was Professor of Medical Microbiology at Stanford University School of Medicine. He is a past President of the Gerontological Society of America and was a founding member of the Council of the National Institute on Aging (NIA). The recipient of several research prizes and awards, including the 1991 Sandoz Prize for Gerontological Research, he has studied the aging process for more than 40 years. He is most well known for discovering that human fibroblast cells divide for a limited number of times in vitro (now known as the "Hayflick Limit" in his honor), refuting the earlier contention by Alexis Carrel that normal body cells are immortal.
Hayflick is the author of the book, How and Why We Age, published by Ballantine Books; 1994. This book has been translated into nine languages and is published in Japan, Brazil, Russia, Spain, Germany, the Czech Republic, Poland, Israel and Hungary. It was a selection of The Book of the Month Club and has sold over 50,000 copies worldwide.
Hayflick and his colleagues have vehemently condemned "anti-aging medicine." Hayflick has written numerous articles criticizing both the feasibility and desirability of human life extension which have provoked responses critical of his views.
Click for References.
Place: Conference Room 159; Boyer
Hall at UCLA
Take the 405 (San Diego Freeway) to Wilshire Blvd. Turn toward Westwood. Turn Left on Westwood Blvd. and then enter into the main campus of UCLA. Drive to the Parking Kiosk in the center median and request parking for Lot No. 9 ($10.00). Turn right and right and enter the gate with a ticket. Go up to the very top at roof-top level and park in the diagonally opposite corner of the structure. Walk up the ramp and to the end. Turn right and left and left. The first tall building on the right is Boyer Hall. Check the sign on the glass of the front door if its locked. Once in the building, take a quick right and left to Conference Room 159.
Click for an interactive map of the campus.
Other Telephone Numbers: Cell: 310-892-9120
Click here for a more detailed list of the topics we normally cover after the main lecture.
Once again, our government has demonstrated a deliberate status-quo strategy in defending its chronologically- challenged constituents. Contrary to the hopes of those who worked so hard to lobby for funding from the Congress to create this agency as a separate division of NIH, naively expecting that it would reveal a true path to the "cutting-edge therapies to come," this agency has become an instrument of oppressive zero-risk conservative geriatric internal medicine. Come and give us your opinion.