Open Thread -- Age and Longetivity Research Edition
The end of the year approaches, and with it comes the promise that we will be yet another year wiser; those who have survived the turbulent ups and downs of the year have also achieved the milestone of becoming yet another year older.
That need not sound as ominous or regretful as it appears.
Research into aging and human longetivity has continued to make strides – yes, even during the rein of the Bush Administration – and promising new results have led to insights not only into the process of aging and longetivity but also into the study of cancer. Below is a cross-section of articles from the past eight years on a few of the findings:
- 5/11/2001 "Protective Protein Caps Discovered At Ends Of Human Chromosomes" -- ScienceDaily (adapted from mat'l provided by Univ. of CO at Boulder)
Howard Hughes Medical Institute and University of Colorado researchers have identified the protective protein "caps" that form the ends of all human chromosomes, a finding that may eventually have applications for cellular aging and human diseases.
The very end of chromosomes, known as telomeres, contain repeating chains of DNA that protect chromosomes from damage, said Peter Baumann, a Howard Hughes Medical Institute researcher working at the University of Colorado at Boulder. Portions of the telomeres are lost each time a cell divides, a process that may act as a biological clock by signaling the cell to stop dividing after a certain point.
- 10/4/2001 "Scientists Make Key Finding Underlying Genetic Stability" -- ScienceDaily (adapted from mat'l provided by Los Alamos National Laboratory, NM)
Biologists at the U.S. Department of Energy's Los Alamos National Laboratory have discovered new insights into how two common proteins found in mammalian cells can cause chromosomes to fuse together -mutations that can destroy cells or give rise to cancer.
The research, by Susan Bailey and Edwin Goodwin of Los Alamos' Biosciences Division, was published recently in the journal Science.
Bailey, Goodwin and their colleagues looked at the role of telomeres in protecting chromosome ends. Chromosomes are made of deoxyribonucleic acid - DNA - and are the carriers of genetic information.
- 2/20/2004 "Biochemical Clues To Long Lifespan Revealed: Findings Extend Longevity Research From Yeast And Worms To Mammals" -- ScienceDaily (adapted from mat'l provided by Children's Hospital, Boston)
Previous studies in yeast and worms pinpointed a gene known as Sir2 as a key regulator of lifespan: deleting Sir2 limits lifespan, and extra copies lengthen it. Sir2 has a counterpart in mammals, but until now, very little was known about how it worked or what it had to do with aging. Working with mouse cells, researchers led by Anne Brunet, a postdoctoral fellow in neuroscience at Children's Hospital who is now at Stanford University, discovered that Sir2 works by regulating a group of proteins known as FOXO transcription factors. FOXO proteins have also been linked with longevity; they control the expression of genes that regulate cell suicide, and also enable the cell to resist oxidative stress, or chemical stresses that can disrupt the cell's DNA, or genetic blueprint.
- 11/18/2005 "Deleting 'Anti-Aging' Gene From Yeast Greatly Lengthens Life Span" -- ScienceDaily (adapted from materials provided by Univ. of So. CA)
A counterintuitive experiment has resulted in one of the longest recorded life-span extensions in any organism and opened a new door for anti-aging research in humans. Scientists have known for several years that an extra copy of the SIR2 gene can promote longevity in yeast, worms and fruit flies.
Now, molecular geneticists at the University of Southern California suggest that SIR2 instead promotes aging.
- 3/14/2007 "Aging Boosts Chances That A Family Line Will Be Long-lived" -- ScienceDaily (adapted from mat'l provided by Univ. of WA)
It is an inevitability of life -- you are born and you begin to age.
Scientists have puzzled over just why organisms evolved aging as a strategy, and now there appears to be an answer. Allowing one individual to carry all the cellular damage inflicted over time, rather than dividing it between two organisms during reproduction, increases the chances that the individual's line will continue to reproduce for many generations to come, a new study indicates.
- 5/4/2007 "Vitamin Extends Life In Yeast, Scientists Find" -- ScienceDaily (Adapted from materials provided by Dartmouth Medical School, via EurekAlert!, a service of AAAS.)
Imagine taking a vitamin for longevity! Not yet, but a Dartmouth discovery that a cousin of niacin prolongs lifespan in yeast brings the tantalizing possibility a step closer.
The research, reported in the May 4 issue of Cell, shows how a new vitamin extends lifespan in yeast cells, much like calorie restriction does in animals. It could pave the way for developing supplements to benefit humans.
- 11/28/2008 "Research on mice links fast food to Alzheimer's" -- Reuters (via NewsDaily)
Mice fed junk food for nine months showed signs of developing the abnormal brain tangles strongly associated with Alzheimer's disease, a Swedish researcher said on Friday.
The findings, which come from a series of published papers by a researcher at Sweden's Karolinska Institutet, show how a diet rich in fat, sugar and cholesterol could increase the risk of the most common type of dementia.
- 11/28/2008 "Scientists find 4 genes that drive metabolism" -- Reuters (via NewsDaily)
Four genetic variations appear to determine the speed at which people burn up food, researchers said on Thursday, a finding that could one day see doctors offer their patients more individual care.
Differences in metabolism can make some people more susceptible to diseases such as diabetes and explain why response to diet, exercise and drugs to treat certain conditions varies from person to person.
- 11/28/2008 "Potentially Universal Mechanism Of Aging Identified" -- ScienceDaily (Adapted from materials provided by Harvard Medical School, via EurekAlert!, a service of AAAS.)
Researchers have uncovered what may be a universal cause of aging, one that applies to both single cell organisms such as yeast and multicellular organisms, including mammals. This is the first time that such an evolutionarily conserved aging mechanism has been identified between such diverse organisms.
The mechanism probably dates back more than one billion years. The study shows how DNA damage eventually leads to a breakdown in the cell's ability to properly regulate which genes are switched on and off in particular settings.
- 11/28/2008 "Rodent of the week: Finding the root cause of aging" -- Shari Roan, Los Angeles Times
Researchers believe they have identified a fundamental cause of aging, according to a study published this week in the journal Cell. The mechanism was previously found in fungus and has now been discovered in mice. It's likely that the same process applies to humans, said the authors of the research, from Harvard.
The study found that DNA damage, which accrues as we age, decreases a cell's ability to regulate which genes are turned on and off in particular settings. Though DNA damage speeds up aging, the actual cause is not the DNA damage but the lack of gene regulation. However, this lack of gene regulation, called epigenetics, may be reversible.
Now that we've stuffed your noggins with all this Science-newsy goodness, stick around a while.
This is an Open Thread.