Source: StemCells, Inc.
Date: October 4, 2012
Summary:
NEWARK, Calif. -- StemCells, Inc. today announced that the first patient in its Phase I/II clinical trial in dry age-related macular degeneration (AMD) has been enrolled and transplanted. The trial is designed to evaluate the safety and preliminary efficacy of the Company's proprietary HuCNS-SC® product candidate (purified human neural stem cells) as a treatment for dry AMD, and the patient was transplanted with the cells yesterday at the Retina Foundation of the Southwest (RFSW) in Dallas, Texas, one of the leading independent vision research centers in the United States. AMD afflicts approximately 30 million people worldwide and is the leading cause of vision loss and blindness in people over 55 years of age.
Showing posts with label aging. Show all posts
Showing posts with label aging. Show all posts
Thursday, October 04, 2012
Wednesday, May 23, 2012
Researchers Develop Method to Delay Aging of Stem Cells
Source: Salk Institute for Biological Studies
Date: May 23, 2012
Summary:
LA JOLLA, CA—Stem cells are essential building blocks for all organisms, from plants to humans. They can divide and renew themselves throughout life, differentiating into the specialized tissues needed during development, as well as cells necessary to repair adult tissue. Therefore, they can be considered immortal, in that they recreate themselves and regenerate tissues throughout a person's lifetime, but that doesn't mean they don't age. They do, gradually losing their ability to effectively maintain tissues and organs.
Now, researchers at the Salk Institute for Biological Studies have uncovered a series of biological events that implicate the stem cells' surroundings, known as their "niche," as the culprit in loss of stem cells due to aging. Their findings, published May 23rd in Nature, have implications for treatment of age-related diseases and for the effectiveness of regenerative medicine.
Date: May 23, 2012
Summary:
LA JOLLA, CA—Stem cells are essential building blocks for all organisms, from plants to humans. They can divide and renew themselves throughout life, differentiating into the specialized tissues needed during development, as well as cells necessary to repair adult tissue. Therefore, they can be considered immortal, in that they recreate themselves and regenerate tissues throughout a person's lifetime, but that doesn't mean they don't age. They do, gradually losing their ability to effectively maintain tissues and organs.
Now, researchers at the Salk Institute for Biological Studies have uncovered a series of biological events that implicate the stem cells' surroundings, known as their "niche," as the culprit in loss of stem cells due to aging. Their findings, published May 23rd in Nature, have implications for treatment of age-related diseases and for the effectiveness of regenerative medicine.
Thursday, May 03, 2012
Aged Hematopoietic Stem Cells Rejuvenated to Be Functionally Younger
Source: Cincinnati Children's Hospital Medical Center
Date: May 3, 2012
Summary:
Researchers have rejuvenated aged hematopoietic stem cells to be functionally younger, offering intriguing clues into how medicine might one day fend off some ailments of old age. Scientists at Cincinnati Children’s Hospital Medical Center and the Ulm University Medicine in Germany report their findings online May 3 in the journal Cell Stem Cell. The paper brings new perspective to what has been a life science controversy – countering what used to be broad consensus that the aging of hematopoietic stem cells (HSCs) was locked in by nature and not reversible by therapeutic intervention.
The findings are early and involve laboratory manipulation of mouse cells, so it remains to be seen what direct application they may have for humans. Still, the study expands what is known about the basic molecular and cellular mechanisms of aging -- a necessary step to one day designing rational approaches to aiding a healthy aging process.
One reason the research team focused on Cdc42 is that previous studies have reported elevated activity of the protein in various tissue types of older mice -- which have a natural life span of around two years. Also, elevated expression of Cdc42 has been found in immune system white blood cells in older humans.
In the current study, researchers found elevated activity of Cdc42 in the HSCs of older mice. They also were able to induce premature aging of HSCs in mice by genetically increasing Cdc42 activity in the cells. The aged cells lost structural organization and polarity, resulting in improper placement and spacing of components inside the cells. This disorganization contributed to the cells' decreased functional efficiency.
Date: May 3, 2012
Summary:
Researchers have rejuvenated aged hematopoietic stem cells to be functionally younger, offering intriguing clues into how medicine might one day fend off some ailments of old age. Scientists at Cincinnati Children’s Hospital Medical Center and the Ulm University Medicine in Germany report their findings online May 3 in the journal Cell Stem Cell. The paper brings new perspective to what has been a life science controversy – countering what used to be broad consensus that the aging of hematopoietic stem cells (HSCs) was locked in by nature and not reversible by therapeutic intervention.
The findings are early and involve laboratory manipulation of mouse cells, so it remains to be seen what direct application they may have for humans. Still, the study expands what is known about the basic molecular and cellular mechanisms of aging -- a necessary step to one day designing rational approaches to aiding a healthy aging process.
One reason the research team focused on Cdc42 is that previous studies have reported elevated activity of the protein in various tissue types of older mice -- which have a natural life span of around two years. Also, elevated expression of Cdc42 has been found in immune system white blood cells in older humans.
In the current study, researchers found elevated activity of Cdc42 in the HSCs of older mice. They also were able to induce premature aging of HSCs in mice by genetically increasing Cdc42 activity in the cells. The aged cells lost structural organization and polarity, resulting in improper placement and spacing of components inside the cells. This disorganization contributed to the cells' decreased functional efficiency.
Friday, March 23, 2012
Embryonic Stem Cells Shift Metabolism in Cancer-Like Way Upon Implanting in Uterus
Source: University of Washington
Date: March 23, 2012
Summary:
Shortly after a mouse embryo starts to form, some of its stem cells undergo a dramatic metabolic shift to enter the next stage of development, University of Washington researchers have reported. These stem cells start using and producing energy like cancer cells. This discovery is recently published in EMBO, the European Molecular Biology Organization journal.
The metabolic transition they discovered occurs very early as the mouse embryo, barely more than a speck of dividing cells, implants in the mother's uterus. The change is driven by low oxygen conditions, Ruohola-Baker explained.
The researchers also saw a specific type of biochemical slowdown in the stem cells' mitochondria -- the cells' powerhouses. The phenomenon previously was associated with aging and disease. This was the first example of the same downshift controlling normal early embryonic development.
Date: March 23, 2012
Summary:
Shortly after a mouse embryo starts to form, some of its stem cells undergo a dramatic metabolic shift to enter the next stage of development, University of Washington researchers have reported. These stem cells start using and producing energy like cancer cells. This discovery is recently published in EMBO, the European Molecular Biology Organization journal.
The metabolic transition they discovered occurs very early as the mouse embryo, barely more than a speck of dividing cells, implants in the mother's uterus. The change is driven by low oxygen conditions, Ruohola-Baker explained.
The researchers also saw a specific type of biochemical slowdown in the stem cells' mitochondria -- the cells' powerhouses. The phenomenon previously was associated with aging and disease. This was the first example of the same downshift controlling normal early embryonic development.
Friday, February 24, 2012
Memory Formation Triggered by Stem Cell Development
Source: RIKEN
Date: February 24, 2012
Summary:
Researchers at the RIKEN-MIT Center for Neural Circuit Genetics have discovered an answer to the long-standing mystery of how brain cells can both remember new memories while also maintaining older ones. They found that specific neurons in a brain region called the dentate gyrus serve distinct roles in memory formation depending on whether the neural stem cells that produced them were of old versus young age. The study will appear in the March 30 issue of Cell and links the cellular basis of memory formation to the birth of new neurons -- a finding that could unlock a new class of drug targets to treat memory disorders. The findings also suggest that an imbalance between young and old neurons in the brain could disrupt normal memory formation during post-traumatic stress disorder (PTSD) and aging.
Date: February 24, 2012
Summary:
Researchers at the RIKEN-MIT Center for Neural Circuit Genetics have discovered an answer to the long-standing mystery of how brain cells can both remember new memories while also maintaining older ones. They found that specific neurons in a brain region called the dentate gyrus serve distinct roles in memory formation depending on whether the neural stem cells that produced them were of old versus young age. The study will appear in the March 30 issue of Cell and links the cellular basis of memory formation to the birth of new neurons -- a finding that could unlock a new class of drug targets to treat memory disorders. The findings also suggest that an imbalance between young and old neurons in the brain could disrupt normal memory formation during post-traumatic stress disorder (PTSD) and aging.
Wednesday, February 22, 2012
Scientists trigger muscle stem cells to divide
Source: Stanford University School of Medicine
Date: February 22, 2012
Summary:
A tiny piece of RNA plays a key role in determining when muscle stem cells from mice activate and start to divide, according to researchers at the Stanford University School of Medicine. The finding may help scientists learn how to prepare human muscle stem cells for use in therapies for conditions such as muscular dystrophy and aging by controlling their activation state.
It’s the first time that a small regulatory RNA, called a microRNA, has been implicated in the maintenance of the adult stem cell resting, or quiescent, state. The research is published Feb. 23 in Nature. Postdoctoral scholar Tom Cheung, PhD, is the first author of the study.
Date: February 22, 2012
Summary:
A tiny piece of RNA plays a key role in determining when muscle stem cells from mice activate and start to divide, according to researchers at the Stanford University School of Medicine. The finding may help scientists learn how to prepare human muscle stem cells for use in therapies for conditions such as muscular dystrophy and aging by controlling their activation state.
It’s the first time that a small regulatory RNA, called a microRNA, has been implicated in the maintenance of the adult stem cell resting, or quiescent, state. The research is published Feb. 23 in Nature. Postdoctoral scholar Tom Cheung, PhD, is the first author of the study.
Monday, February 06, 2012
Researchers develop method of directing stem cells to increase bone formation and bone strength
Source: University of California - Davis
Date: February 6, 2012
Summary:
A research team led by UC Davis Health System scientists has developed a novel technique to enhance bone growth by using a molecule which, when injected into the bloodstream, directs the body's stem cells to travel to the surface of bones. Once these cells are guided to the bone surface by this molecule, the stem cells differentiate into bone-forming cells and synthesize proteins to enhance bone growth. The study, which was published online today in Nature Medicine, used a mouse model of osteoporosis to demonstrate a unique treatment approach that increases bone density and prevents bone loss associated with aging and estrogen deficiency.
Date: February 6, 2012
Summary:
A research team led by UC Davis Health System scientists has developed a novel technique to enhance bone growth by using a molecule which, when injected into the bloodstream, directs the body's stem cells to travel to the surface of bones. Once these cells are guided to the bone surface by this molecule, the stem cells differentiate into bone-forming cells and synthesize proteins to enhance bone growth. The study, which was published online today in Nature Medicine, used a mouse model of osteoporosis to demonstrate a unique treatment approach that increases bone density and prevents bone loss associated with aging and estrogen deficiency.
Monday, January 30, 2012
StemCells, Inc. Announces Publication of Preclinical Data Demonstrating Its Human Neural Stem Cells Preserve Vision
Source: StemCells, Inc.
Date: January 30, 2012
Summary:
StemCells, Inc. today announced the publication of preclinical data demonstrating that its proprietary HuCNS-SC® cells (purified human neural stem cells) protect host photoreceptors and preserve vision in an animal model of retinal disease. The preclinical results are highly relevant to human disorders of vision loss, the most notable of which is dry age-related macular degeneration (AMD). The study and will be featured as the cover article in the February issue of the international peer-reviewed European Journal of Neuroscience. The results of the study show that photoreceptors, the key cells of the eye involved in vision, were protected from degeneration following transplantation of HuCNS-SC cells into the Royal College of Surgeons (RCS) rat.
Date: January 30, 2012
Summary:
StemCells, Inc. today announced the publication of preclinical data demonstrating that its proprietary HuCNS-SC® cells (purified human neural stem cells) protect host photoreceptors and preserve vision in an animal model of retinal disease. The preclinical results are highly relevant to human disorders of vision loss, the most notable of which is dry age-related macular degeneration (AMD). The study and will be featured as the cover article in the February issue of the international peer-reviewed European Journal of Neuroscience. The results of the study show that photoreceptors, the key cells of the eye involved in vision, were protected from degeneration following transplantation of HuCNS-SC cells into the Royal College of Surgeons (RCS) rat.
Tuesday, January 03, 2012
A Shot of Young Stem Cells Made Rapidly Aging Mice Live Longer and Healthier, Pitt Team Says
Source: University of Pittsburgh School of Medicine
Date: January 3, 2012
Summary:
PITTSBURGH – Mice bred to age too quickly seemed to have sipped from the fountain of youth after scientists at the University of Pittsburgh School of Medicine injected them with stem cell-like progenitor cells derived from the muscle of young, healthy animals. Instead of becoming infirm and dying early as untreated mice did, animals that got the stem/progenitor cells improved their health and lived two to three times longer than expected, according to findings published in the Jan. 3 edition of Nature Communications.
ABC News, MSNBC, The Daily Mail and the Pittsburgh Tribune-Review carried news stories today on this development.
Date: January 3, 2012
Summary:
PITTSBURGH – Mice bred to age too quickly seemed to have sipped from the fountain of youth after scientists at the University of Pittsburgh School of Medicine injected them with stem cell-like progenitor cells derived from the muscle of young, healthy animals. Instead of becoming infirm and dying early as untreated mice did, animals that got the stem/progenitor cells improved their health and lived two to three times longer than expected, according to findings published in the Jan. 3 edition of Nature Communications.
ABC News, MSNBC, The Daily Mail and the Pittsburgh Tribune-Review carried news stories today on this development.
Wednesday, December 07, 2011
Research could help people with declining sense of smell
Source: University of California - Berkeley
Date: December 7, 2011
Summary:
University of California, Berkeley, neuroscientists have discovered a genetic trigger that makes the nose renew its smell sensors, providing hope for new therapies for people who have lost their sense of smell due to trauma or old age. The gene tells olfactory stem cells ‑ the adult tissue stem cells in the nose ‑ to mature into the sensory neurons that detect odors and relay that information to the brain. The discovery may also help scientists harness olfactory stem cells and stem cells found in other sensory systems more generally, to recover sensory function following injury or degenerative disease, scientists said. The findings are published in the Dec. 8 issue of the journal Neuron.
Date: December 7, 2011
Summary:
University of California, Berkeley, neuroscientists have discovered a genetic trigger that makes the nose renew its smell sensors, providing hope for new therapies for people who have lost their sense of smell due to trauma or old age. The gene tells olfactory stem cells ‑ the adult tissue stem cells in the nose ‑ to mature into the sensory neurons that detect odors and relay that information to the brain. The discovery may also help scientists harness olfactory stem cells and stem cells found in other sensory systems more generally, to recover sensory function following injury or degenerative disease, scientists said. The findings are published in the Dec. 8 issue of the journal Neuron.
Wednesday, November 23, 2011
Key to Aging? Key Molecular Switch for Telomere Extension by Telomerase Identified
Source: University of Illinois at Chicago
Date: November 23, 2011
Summary:
Researchers at the University of Illinois at Chicago College of Medicine describe for the first time a key target of DNA damage checkpoint enzymes that must be chemically modified to enable stable maintenance of chromosome ends by telomerase, an enzyme thought to play a key role in cancer and aging. Their findings are reported online in Nature Structural and Molecular Biology.
Date: November 23, 2011
Summary:
Researchers at the University of Illinois at Chicago College of Medicine describe for the first time a key target of DNA damage checkpoint enzymes that must be chemically modified to enable stable maintenance of chromosome ends by telomerase, an enzyme thought to play a key role in cancer and aging. Their findings are reported online in Nature Structural and Molecular Biology.
Labels:
aging,
biology,
cancer,
cell division,
enzyme,
genomics,
molecular medicine,
tumors
Thursday, October 27, 2011
Erasing Signs of Aging in Human Cells Now a Reality
Source: INSERM (Institut national de la santé et de la recherche médicale)
Date: October 27, 2011
Summary:
Scientists have recently succeeded in rejuvenating cells from elderly donors (aged over 100). These old cells were reprogrammed in vitro to induced pluripotent stem cells (iPSC) and to rejuvenated and human embryonic stem cells (hESC): cells of all types can again be differentiated after this genuine "rejuvenation" therapy. The results represent significant progress for research into iPSC cells and a further step forwards for regenerative medicine.
Inserm's AVENIR "Genomic plasticity and aging" team, directed by Jean-Marc Lemaitre, Inserm researcher at the Functional Genomics Institute (Inserm/CNRS/Université de Montpellier 1 and 2) performed the research. The results were published in Genes & Development on November 1, 2011.
Date: October 27, 2011
Summary:
Scientists have recently succeeded in rejuvenating cells from elderly donors (aged over 100). These old cells were reprogrammed in vitro to induced pluripotent stem cells (iPSC) and to rejuvenated and human embryonic stem cells (hESC): cells of all types can again be differentiated after this genuine "rejuvenation" therapy. The results represent significant progress for research into iPSC cells and a further step forwards for regenerative medicine.
Inserm's AVENIR "Genomic plasticity and aging" team, directed by Jean-Marc Lemaitre, Inserm researcher at the Functional Genomics Institute (Inserm/CNRS/Université de Montpellier 1 and 2) performed the research. The results were published in Genes & Development on November 1, 2011.
Tuesday, September 20, 2011
Scientists Turn Back the Clock On Adult Stem Cells Aging
Source: Georgia Institute of Technology
Date: September 20, 2011
Summary:
Atlanta, GA - Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Date: September 20, 2011
Summary:
Atlanta, GA - Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases. A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Monday, September 19, 2011
Scientists Turn Back the Clock on Adult Stem Cells Aging
Source: Buck Institute for Research on Aging
Date: September 19, 2011
Summary:
Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Date: September 19, 2011
Summary:
Researchers have shown they can reverse the aging process for human adult stem cells, which are responsible for helping old or damaged tissues regenerate. The findings could lead to medical treatments that may repair a host of ailments that occur because of tissue damage as people age. A research group led by the Buck Institute for Research on Aging and the Georgia Institute of Technology conducted the study in cell culture, which appears in the September 1, 2011 edition of the journal Cell Cycle.
The regenerative power of tissues and organs declines as we age. The modern day stem cell hypothesis of aging suggests that living organisms are as old as are its tissue specific or adult stem cells. Therefore, an understanding of the molecules and processes that enable human adult stem cells to initiate self-renewal and to divide, proliferate and then differentiate in order to rejuvenate damaged tissue might be the key to regenerative medicine and an eventual cure for many age-related diseases A research group led by the Buck Institute for Research on Aging in collaboration with the Georgia Institute of Technology, conducted the study that pinpoints what is going wrong with the biological clock underlying the limited division of human adult stem cells as they age.
Wednesday, August 31, 2011
Scientists discover blood factors that appear to cause aging in brains of mice
Source: Stanford University School of Medicine
Date: August 31, 2011
Summary:
In a study to be published Sept. 1 in Nature, Stanford University School of Medicine scientists have found substances in the blood of old mice that makes young brains act older. These substances, whose levels rise with increasing age, appear to inhibit the brain's ability to produce new nerve cells critical to memory and learning. The scientists believe the findings raise the question of whether it might be possible to shield the brain from aging by eliminating or mitigating the effects of these apparently detrimental blood-borne substances, or perhaps by identifying other blood-borne substances that exert rejuvenating effects on the brain but whose levels decline with age,
Date: August 31, 2011
Summary:
In a study to be published Sept. 1 in Nature, Stanford University School of Medicine scientists have found substances in the blood of old mice that makes young brains act older. These substances, whose levels rise with increasing age, appear to inhibit the brain's ability to produce new nerve cells critical to memory and learning. The scientists believe the findings raise the question of whether it might be possible to shield the brain from aging by eliminating or mitigating the effects of these apparently detrimental blood-borne substances, or perhaps by identifying other blood-borne substances that exert rejuvenating effects on the brain but whose levels decline with age,
Wednesday, July 13, 2011
Researchers Demystify a Fountain of Youth in the Adult Brain
Source: Duke University Medical Center
Date: July 13, 2011
Summary:
Duke University Medical Center researchers have found that a “fountain of youth” that sustains the production of new neurons in the brains of rodents is also believed to be present in the human brain. The existence of a vital support system of cells around stem cells in the brain explains why stem cells by themselves can’t generate neurons in a lab dish, a major roadblock in using these stem cells for injury repair. The study is the cover story in the July issue of Neuron, published online July 14.
Date: July 13, 2011
Summary:
Duke University Medical Center researchers have found that a “fountain of youth” that sustains the production of new neurons in the brains of rodents is also believed to be present in the human brain. The existence of a vital support system of cells around stem cells in the brain explains why stem cells by themselves can’t generate neurons in a lab dish, a major roadblock in using these stem cells for injury repair. The study is the cover story in the July issue of Neuron, published online July 14.
Tuesday, June 14, 2011
New Research Provides Clues on Why Hair Turns Gray Communication Between Hair Follicles and Melanocyte Stem Cells Key to Mystery
Source: NYU Langone Medical Center / New York University School of Medicine
Date: June 14, 2011
Summary:
A new study by researchers at NYU Langone Medical Center has shown that, for the first time, Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation. The study was published in the June 11, 2011 issue of the journal Cell. Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color. Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair.
Date: June 14, 2011
Summary:
A new study by researchers at NYU Langone Medical Center has shown that, for the first time, Wnt signaling, already known to control many biological processes, between hair follicles and melanocyte stem cells can dictate hair pigmentation. The study was published in the June 11, 2011 issue of the journal Cell. Using genetic mouse models, researchers were able to examine how Wnt signaling pathways enabled both hair follicle stem cells and melanocyte stem cells to work together to generate hair growth and produce hair color. Research also showed the depletion (or inhibition or abnormal) Wnt signaling in hair follicle stem cells not only inhibits hair re-growth but also prevents melanocytes stem cell activation required for producing hair color. The lack of Wnt activation in melanocyte stem cells leads to depigmented or gray hair.
Thursday, June 09, 2011
Researchers work to turn back the clock on bone-producing stem cells
Source: Georgia Health Sciences University
Date: June 9, 2011
Summary:
AUGUSTA, Ga. – Researchers want to turn back the clock on aging stem cells so they’ll make better bone. Bone-weakening osteoporosis results in a fracture every three seconds worldwide, according to the International Osteoporosis Foundation. The right nutrients resulting in the right signals could help aging stem cells act more youthful, producing stronger bones longer and reducing the death and disability associated with a frail framework, Georgia Health Sciences University researchers say.
Date: June 9, 2011
Summary:
AUGUSTA, Ga. – Researchers want to turn back the clock on aging stem cells so they’ll make better bone. Bone-weakening osteoporosis results in a fracture every three seconds worldwide, according to the International Osteoporosis Foundation. The right nutrients resulting in the right signals could help aging stem cells act more youthful, producing stronger bones longer and reducing the death and disability associated with a frail framework, Georgia Health Sciences University researchers say.
Monday, May 16, 2011
Stem cell study could pave the way to treatment for age-related muscle wasting
Source: Monash University
Date: 16 May 2011
Summary:
A team led by Monash University developmental biologist Professor Christophe Marcelle has nailed the mechanism that causes stem cells in the embryo to differentiate into specialised cells that form the skeletal muscles of animals’ bodies. The scientists published their results in the British journal Nature on Monday (May 16).
The researchers analysed the differentiation of muscle stem cells in chicken embryos. The mechanisms in birds are identical to those in mammals, so the chick is a good model species for understanding the mechanisms in humans.
The scientists investigated the effect of a known signalling pathway called NOTCH on muscle differentiation. They found that differentiation of stem cells to muscle was initiated when NOTCH signalling proteins touched some of the cells. These proteins were carried by passing cells migrating from a different tissue–the neural crest–the progenitor tissue of sensory nerve cells. Muscle formation in the target stem cells occurred only when the NOTCH pathway was triggered briefly by the migrating neural crest cells.
Date: 16 May 2011
Summary:
A team led by Monash University developmental biologist Professor Christophe Marcelle has nailed the mechanism that causes stem cells in the embryo to differentiate into specialised cells that form the skeletal muscles of animals’ bodies. The scientists published their results in the British journal Nature on Monday (May 16).
The researchers analysed the differentiation of muscle stem cells in chicken embryos. The mechanisms in birds are identical to those in mammals, so the chick is a good model species for understanding the mechanisms in humans.
The scientists investigated the effect of a known signalling pathway called NOTCH on muscle differentiation. They found that differentiation of stem cells to muscle was initiated when NOTCH signalling proteins touched some of the cells. These proteins were carried by passing cells migrating from a different tissue–the neural crest–the progenitor tissue of sensory nerve cells. Muscle formation in the target stem cells occurred only when the NOTCH pathway was triggered briefly by the migrating neural crest cells.
Thursday, May 05, 2011
Study identifies stem cell-related changes that may contribute to age-related cognitive decline
Source: Cold Spring Harbor Laboratory
Date: May 5, 2011
Summary:
Cold Spring Harbor, N.Y. – A new study from Cold Spring Harbor Laboratory (CSHL) offers an explanation for why our brains produce fewer and fewer neurons with age, a phenomenon thought to underlie age-related cognitive decline. The study, published as the cover story in the May 6 issue of Cell Stem Cell, suggests that this drop in production is due to the shrinking cache of adult stem cells in our brains.
Date: May 5, 2011
Summary:
Cold Spring Harbor, N.Y. – A new study from Cold Spring Harbor Laboratory (CSHL) offers an explanation for why our brains produce fewer and fewer neurons with age, a phenomenon thought to underlie age-related cognitive decline. The study, published as the cover story in the May 6 issue of Cell Stem Cell, suggests that this drop in production is due to the shrinking cache of adult stem cells in our brains.
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