Source: Cedars-Sinai Medical Center
Date: June 19, 2012
Summary:
LOS ANGELES – Cedars-Sinai’s Regenerative Medicine Institute has pioneered research on how motor-neuron cell-death occurs in patients with spinal muscular atrophy, offering an important clue in identifying potential medicines to treat this leading genetic cause of death in infants and toddlers. The study, published in the June 19 online issue of PLoS ONE, extends the institute’s work to employ pluripotent stem cells to find a pharmaceutical treatment for spinal muscular atrophy or SMA, a genetic neuromuscular disease characterized by muscle atrophy and weakness.
Showing posts with label cell death. Show all posts
Showing posts with label cell death. Show all posts
Tuesday, June 19, 2012
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.
Tuesday, January 04, 2011
Malfunctioning Gene Associated With Lou Gehrig's Disease Leads to Nerve-Cell Death in Mice
Source: University of Pennsylvania School of Medicine
Date: January 4, 2011
Summary:
Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD) are characterized by protein clumps in brain and spinal-cord cells that include an RNA-binding protein called TDP-43. This protein is the major building block of the lesions formed by these clumps.
In a study published in the Journal of Clinical Investigation, a team led by Virginia M.-Y. Lee, PhD, director of Penn's Center for Neurodegenerative Disease Research, describes the first direct evidence of how mutated TDP-43 can cause neurons to die. Although normally found in the nucleus where it regulates gene expression, TDP-43 was first discovered in 2006 to be the major disease protein in ALS and FTLD by the Penn team led by Lee and John Q. Trojanowski, MD, PhD, director of the Institute on Aging at Penn. This discovery has transformed research on ALS and FTLD by linking them to the same disease protein.
Date: January 4, 2011
Summary:
Lou Gehrig's disease, or amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD) are characterized by protein clumps in brain and spinal-cord cells that include an RNA-binding protein called TDP-43. This protein is the major building block of the lesions formed by these clumps.
In a study published in the Journal of Clinical Investigation, a team led by Virginia M.-Y. Lee, PhD, director of Penn's Center for Neurodegenerative Disease Research, describes the first direct evidence of how mutated TDP-43 can cause neurons to die. Although normally found in the nucleus where it regulates gene expression, TDP-43 was first discovered in 2006 to be the major disease protein in ALS and FTLD by the Penn team led by Lee and John Q. Trojanowski, MD, PhD, director of the Institute on Aging at Penn. This discovery has transformed research on ALS and FTLD by linking them to the same disease protein.
Thursday, October 14, 2010
Gene identified that prevents stem cells from turning cancerous
Source: Rockefeller University
Date: October 14, 2010
Summary:
Stem cells, the prodigious precursors of all the tissues in our body, can make almost anything, given the right circumstances. Including, unfortunately, cancer. Now research from Rockefeller University shows that having too many stem cells, or stem cells that live for too long, can increase the odds of developing cancer. By identifying a mechanism that regulates programmed cell death in precursor cells for blood, or hematopoietic stem cells, the work is the first to connect the death of such cells to a later susceptibility to tumors in mice. It also provides evidence of the potentially carcinogenic downside to stem cell treatments, and suggests that nature has sought to balance stem cells' regenerative power against their potentially lethal potency.
Researchers explored the activity of a gene called Sept4, which encodes a protein, ARTS, that increases programmed cell death, or apoptosis, by antagonizing other proteins that prevent cell death. ARTS is found to be lacking in human leukemia and other cancers, suggesting it suppresses tumors. To study the role of ARTS, the experimenters bred a line of mice genetically engineered to lack the Sept4 gene.
Researchers studied cells that lacked ARTS, looking for signs of trouble relating to cell death. In mature B and T cells, she could not find any, however, so she began to look at cells earlier and earlier in development, until finally she was comparing hematopoietic progenitor and stem cells. Here she found crucial differences, to be published Friday in Genes and Development.
Date: October 14, 2010
Summary:
Stem cells, the prodigious precursors of all the tissues in our body, can make almost anything, given the right circumstances. Including, unfortunately, cancer. Now research from Rockefeller University shows that having too many stem cells, or stem cells that live for too long, can increase the odds of developing cancer. By identifying a mechanism that regulates programmed cell death in precursor cells for blood, or hematopoietic stem cells, the work is the first to connect the death of such cells to a later susceptibility to tumors in mice. It also provides evidence of the potentially carcinogenic downside to stem cell treatments, and suggests that nature has sought to balance stem cells' regenerative power against their potentially lethal potency.
Researchers explored the activity of a gene called Sept4, which encodes a protein, ARTS, that increases programmed cell death, or apoptosis, by antagonizing other proteins that prevent cell death. ARTS is found to be lacking in human leukemia and other cancers, suggesting it suppresses tumors. To study the role of ARTS, the experimenters bred a line of mice genetically engineered to lack the Sept4 gene.
Researchers studied cells that lacked ARTS, looking for signs of trouble relating to cell death. In mature B and T cells, she could not find any, however, so she began to look at cells earlier and earlier in development, until finally she was comparing hematopoietic progenitor and stem cells. Here she found crucial differences, to be published Friday in Genes and Development.
Tuesday, September 07, 2010
Researchers at UC Riverside Find Solution to Cell Death Problem Vexing Stem Cell Research
University of California - Riverside
Date: September 7, 2010
Summary:
RIVERSIDE, Calif. – Human pluripotent stem (hPS) cells can generate any given cell type in the adult human body, which is why they are of interest to stem cell scientists working on finding therapies for spinal cord injuries, Parkinson's disease, burns, heart disease, diabetes, arthritis, and other ailments. Before hPS cell technologies can be translated into clinical applications, however, some obstacles must first be overcome.
One such obstacle frustrating stem cell researchers is “cell death” that the major types of hPS cells, including human embryonic stem cells and human induced pluripotent stem cells, mysteriously undergo when cultured as single cells, rendering them less suitable for research.
Researchers at the University of California, Riverside now show that a molecular motor, called “nonmuscle myosin II” (NMII), which exists naturally inside each hPS cell and controls various cellular functions, triggers the death of hPS cells when they are broken down to single cells.
While many details of how exactly NMII works remain unknown, a wide consensus among researchers is that NMII induces a contraction of the main internal components of the cells, eventually resulting in cell death. To stop this cell death, the researchers treated hPS cells with a chemically synthesized compound, blebbistatin, and found that it substantially enhanced the survival of the cells by chemically inhibiting NMII. (Blebbistatin is commercially available from several companies that sell biologically active chemical compounds.)
Study results appear online, Sept. 7, in Nature Communications.
Date: September 7, 2010
Summary:
RIVERSIDE, Calif. – Human pluripotent stem (hPS) cells can generate any given cell type in the adult human body, which is why they are of interest to stem cell scientists working on finding therapies for spinal cord injuries, Parkinson's disease, burns, heart disease, diabetes, arthritis, and other ailments. Before hPS cell technologies can be translated into clinical applications, however, some obstacles must first be overcome.
One such obstacle frustrating stem cell researchers is “cell death” that the major types of hPS cells, including human embryonic stem cells and human induced pluripotent stem cells, mysteriously undergo when cultured as single cells, rendering them less suitable for research.
Researchers at the University of California, Riverside now show that a molecular motor, called “nonmuscle myosin II” (NMII), which exists naturally inside each hPS cell and controls various cellular functions, triggers the death of hPS cells when they are broken down to single cells.
While many details of how exactly NMII works remain unknown, a wide consensus among researchers is that NMII induces a contraction of the main internal components of the cells, eventually resulting in cell death. To stop this cell death, the researchers treated hPS cells with a chemically synthesized compound, blebbistatin, and found that it substantially enhanced the survival of the cells by chemically inhibiting NMII. (Blebbistatin is commercially available from several companies that sell biologically active chemical compounds.)
Study results appear online, Sept. 7, in Nature Communications.
Wednesday, September 01, 2010
Biologists find way to reduce stem cell loss during cancer treatment
Source: University of California - San Diego
Date: September 5, 2010
Summary:
Biologists at the University of California, San Diego have discovered that a gene critical for programmed cell death is also important in the loss of adult stem cells, a finding that could help to improve the health and well-being of patients undergoing cancer treatment. The findings are published in this week's advance online issue of the journal Nature Cell Biology.
Scientists have long known that when normal cells accumulate significant amount of DNA damage, such as during cancer therapy, the tumor suppressor p53 is activated, which leads cells to stop dividing, go into hibernation and undergo a programmed cell death called apoptosis. They've also known that a gene called Puma, an acronym for "p53-unregulated modulator of apoptosis," is critical for p53 to initiate the cell death of DNA-damaged cells.
Using genetically modified mice with persistently activated p53, Xu and his colleagues discovered that, once activated, p53 depletes various adult stem cells, including the ones that are responsible for generating new blood and intestine cells. In addition, Puma is critical for this p53-dependent depletion of various adult stem cells.
Date: September 5, 2010
Summary:
Biologists at the University of California, San Diego have discovered that a gene critical for programmed cell death is also important in the loss of adult stem cells, a finding that could help to improve the health and well-being of patients undergoing cancer treatment. The findings are published in this week's advance online issue of the journal Nature Cell Biology.
Scientists have long known that when normal cells accumulate significant amount of DNA damage, such as during cancer therapy, the tumor suppressor p53 is activated, which leads cells to stop dividing, go into hibernation and undergo a programmed cell death called apoptosis. They've also known that a gene called Puma, an acronym for "p53-unregulated modulator of apoptosis," is critical for p53 to initiate the cell death of DNA-damaged cells.
Using genetically modified mice with persistently activated p53, Xu and his colleagues discovered that, once activated, p53 depletes various adult stem cells, including the ones that are responsible for generating new blood and intestine cells. In addition, Puma is critical for this p53-dependent depletion of various adult stem cells.
Monday, April 12, 2010
Scripps Research scientists solve mystery of fragile stem cells
Source: The Scripps Research Institute
Date: April 12, 2010
Summary:
Scientists at The Scripps Research Institute have solved the decade-old mystery of why human embryonic stem cells are so difficult to culture in the laboratory, providing scientists with useful new techniques and moving the field closer to the day when stem cells can be used for therapeutic purposes. The research is being published in the journal Proceedings of the National Academy of Sciences during the week of April 12, 2010.
In the study, the team discovered two novel synthetic small molecule drugs that can be added to human stem cell culture that each individually prevent the death of these cells. The team also unravels the mechanisms by which the compounds promote stem cell survival, shedding light on a previously unknown aspect of stem cell biology. The hope of most researchers in the field is that one day it will be possible to use stem cells — which possess the ability to develop into many other distinct cell types, such as nerve, heart, or lung cells — to repair damaged tissue from any number of diseases, from Type 1 diabetes to Parkinson's disease, as well as from injuries.
Date: April 12, 2010
Summary:
Scientists at The Scripps Research Institute have solved the decade-old mystery of why human embryonic stem cells are so difficult to culture in the laboratory, providing scientists with useful new techniques and moving the field closer to the day when stem cells can be used for therapeutic purposes. The research is being published in the journal Proceedings of the National Academy of Sciences during the week of April 12, 2010.
In the study, the team discovered two novel synthetic small molecule drugs that can be added to human stem cell culture that each individually prevent the death of these cells. The team also unravels the mechanisms by which the compounds promote stem cell survival, shedding light on a previously unknown aspect of stem cell biology. The hope of most researchers in the field is that one day it will be possible to use stem cells — which possess the ability to develop into many other distinct cell types, such as nerve, heart, or lung cells — to repair damaged tissue from any number of diseases, from Type 1 diabetes to Parkinson's disease, as well as from injuries.
Thursday, March 11, 2010
Discovery of Cellular "Switch" May Provide New Means of Triggering Cell Death, Treating Human Diseases
Source: University of Colorado at Boulder
Date: March 11, 2010
Summary:
The discovery of a novel cellular “switch” in the popular laboratory research worm, C. elegans, by a University of Colorado at Boulder team may provide researchers with a new means of triggering programmed cell death in humans to treat disease.
A research team led by the University of Colorado at Boulder has discovered a previously unknown cellular "switch" that may provide researchers with a new means of triggering programmed cell death, findings with implications for treating cancer.
The new results are a big step forward in understanding programmed cell death, or apoptosis, a cell suicide process that involves a series of biochemical events leading to changes like cell body shrinkage, mitochondria destruction and chromosome fragmentation, said CU-Boulder Professor Ding Xue. But unlike traumatic cell death from injury, programmed cell death is a naturally occurring aspect of animal development that may help prevent human diseases like cancer and autoimmune disorders, said Xue, lead author on the new study.
Date: March 11, 2010
Summary:
The discovery of a novel cellular “switch” in the popular laboratory research worm, C. elegans, by a University of Colorado at Boulder team may provide researchers with a new means of triggering programmed cell death in humans to treat disease.
A research team led by the University of Colorado at Boulder has discovered a previously unknown cellular "switch" that may provide researchers with a new means of triggering programmed cell death, findings with implications for treating cancer.
The new results are a big step forward in understanding programmed cell death, or apoptosis, a cell suicide process that involves a series of biochemical events leading to changes like cell body shrinkage, mitochondria destruction and chromosome fragmentation, said CU-Boulder Professor Ding Xue. But unlike traumatic cell death from injury, programmed cell death is a naturally occurring aspect of animal development that may help prevent human diseases like cancer and autoimmune disorders, said Xue, lead author on the new study.
Tuesday, May 13, 2008
Researchers uncover mechanism of action of antibiotic able to reduce neuronal cell death in brain
Source: Virginia Commonwealth University
Date: May 13, 2008
Summary:
Virginia Commonwealth University researchers have discovered how an antibiotic works to modulate the activity of a neurotransmitter that regulates brain functions, which eventually could lead to therapies to treat Alzheimer’s disease, Huntington’s disease, epilepsy, stroke, dementia and malignant gliomas.
Date: May 13, 2008
Summary:
Virginia Commonwealth University researchers have discovered how an antibiotic works to modulate the activity of a neurotransmitter that regulates brain functions, which eventually could lead to therapies to treat Alzheimer’s disease, Huntington’s disease, epilepsy, stroke, dementia and malignant gliomas.
Tuesday, March 11, 2008
Biologists identify key protein in cell's 'self-eating' function
Source: University of California - San Diego
Date: March 11, 2008
Summary:
Molecular biologists at the University of California, San Diego have found one piece of the complex puzzle of autophagy, the process of “self-eating” performed by all eukaryotic cells -- cells with a nucleus -- to keep themselves healthy. Their finding, published in the March 11 issue of the journal Developmental Cell, is important because it allows scientists to control this one aspect of cellular autophagy, and may lead to the ability to control other selective “self-eating” processes. This, in turn, could help illuminate autophagy’s role in aging, immunity, neurodegeneration and cancer.
Date: March 11, 2008
Summary:
Molecular biologists at the University of California, San Diego have found one piece of the complex puzzle of autophagy, the process of “self-eating” performed by all eukaryotic cells -- cells with a nucleus -- to keep themselves healthy. Their finding, published in the March 11 issue of the journal Developmental Cell, is important because it allows scientists to control this one aspect of cellular autophagy, and may lead to the ability to control other selective “self-eating” processes. This, in turn, could help illuminate autophagy’s role in aging, immunity, neurodegeneration and cancer.
Friday, February 29, 2008
Key Step In Programmed Cell Death Discovered
Source: St. Jude Children's Research Hospital
Date: February 29, 2008
Summary:
Investigators have discovered a dance of proteins that protects certain cells from undergoing apoptosis, also known as programmed cell death. Understanding the fine points of apoptosis is important to researchers seeking ways to control this process. In a series of experiments, St. Jude researchers found that if any one of three molecules is missing, certain cells lose the ability to protect themselves from apoptosis. A report on this work appears in the advance online publication of Nature.
Date: February 29, 2008
Summary:
Investigators have discovered a dance of proteins that protects certain cells from undergoing apoptosis, also known as programmed cell death. Understanding the fine points of apoptosis is important to researchers seeking ways to control this process. In a series of experiments, St. Jude researchers found that if any one of three molecules is missing, certain cells lose the ability to protect themselves from apoptosis. A report on this work appears in the advance online publication of Nature.
Monday, November 12, 2007
Developing Drugs To Limit Massive Cell Death After Spinal Cord Injury
Source: Helmholtz Association
Date: November 12, 2007
Summary:
Neurons die 'en masse' when the spinal cord is injured or when a person suffers a stroke. Researchers have now unraveled the molecular mechanism which causes the death not only of damaged neurons, but also of healthy nerve cells. In animal experiments, they have now been able to demonstrate that neuronal cell death can be reduced when the gene of one the key players in this process is knocked out.
Date: November 12, 2007
Summary:
Neurons die 'en masse' when the spinal cord is injured or when a person suffers a stroke. Researchers have now unraveled the molecular mechanism which causes the death not only of damaged neurons, but also of healthy nerve cells. In animal experiments, they have now been able to demonstrate that neuronal cell death can be reduced when the gene of one the key players in this process is knocked out.
Monday, September 17, 2007
Cell death in sparrow brains may provide clues in age-related human diseases
Source: University of Washington
Date: September 17, 2007
Summary:
A remarkable change takes place in the brains of tiny songbirds every year, and some day the mechanism controlling that change may help researchers develop treatments for age-related degenerative diseases of the brain such as Parkinson's and dementia.
Date: September 17, 2007
Summary:
A remarkable change takes place in the brains of tiny songbirds every year, and some day the mechanism controlling that change may help researchers develop treatments for age-related degenerative diseases of the brain such as Parkinson's and dementia.
Thursday, July 05, 2007
Tracing Parkinson's lethal mechanism
Source: Cell Press
Date: July 5, 2007
Summary:
In the vast majority of Parkinson’s disease (PD) patients, the disorder arises not because of a genetic defect, but because some external insult triggers the death of dopamine-producing neurons. Now, researchers have reported progress in understanding the mechanism underlying that death, which they say suggests a new treatment pathway.
Date: July 5, 2007
Summary:
In the vast majority of Parkinson’s disease (PD) patients, the disorder arises not because of a genetic defect, but because some external insult triggers the death of dopamine-producing neurons. Now, researchers have reported progress in understanding the mechanism underlying that death, which they say suggests a new treatment pathway.
Monday, May 21, 2007
Parkinson's protein protects neurons from stress induced cell death
Source: GSF - National Research Center for Environment and Health
Date: May 21, 2007
Summary:
Parkinson’s disease, also known as shaking palsy, is one of the most frequent diseases of the nervous system. Cell death of neurons in specific regions of the midbrain is leading to the onset of the disease. However, the the causes for this extensive cell death are unknown. Especially in cases of early manifestation of the disease mutations in the so-called parkin gene are of great significance. German scientists have now been able to reveal a novel function for the Parkin protein. The scientists could show that Parkin prevents the induction of neuronal cell death. As reported in the Journal of Neuroscience, the protein activates a survival mechanism which had been known for its prominent role in immune response.
Date: May 21, 2007
Summary:
Parkinson’s disease, also known as shaking palsy, is one of the most frequent diseases of the nervous system. Cell death of neurons in specific regions of the midbrain is leading to the onset of the disease. However, the the causes for this extensive cell death are unknown. Especially in cases of early manifestation of the disease mutations in the so-called parkin gene are of great significance. German scientists have now been able to reveal a novel function for the Parkin protein. The scientists could show that Parkin prevents the induction of neuronal cell death. As reported in the Journal of Neuroscience, the protein activates a survival mechanism which had been known for its prominent role in immune response.
Monday, April 30, 2007
Sentry enzyme blocks paths to Parkinson's disease
Source: St. Jude Children's Research Hospital
Date: April 30, 2007
Summary:
The degeneration of brain cells that occurs in Parkinson's disease may be caused by either externally provoked cell death or internally initiated suicide when the molecule that normally prevents these fatal alternatives is missing, according to studies in mouse models by investigators at St. Jude Children's Research Hospital.
Date: April 30, 2007
Summary:
The degeneration of brain cells that occurs in Parkinson's disease may be caused by either externally provoked cell death or internally initiated suicide when the molecule that normally prevents these fatal alternatives is missing, according to studies in mouse models by investigators at St. Jude Children's Research Hospital.
Thursday, March 29, 2007
Researchers identify critical receptor in liver regeneration
Source: University of California - San Diego
Date: March 29, 2007
Summary:
In studies in mouse models, researchers at the University of California, San Diego (UCSD) School of Medicine have found that a cellular receptor involved in triggering cell death is also a necessary component of tissue repair and regeneration immediately following liver injury. This discovery could have implications for early intervention or therapy in liver disease such as cirrhosis or hepatitis.
Date: March 29, 2007
Summary:
In studies in mouse models, researchers at the University of California, San Diego (UCSD) School of Medicine have found that a cellular receptor involved in triggering cell death is also a necessary component of tissue repair and regeneration immediately following liver injury. This discovery could have implications for early intervention or therapy in liver disease such as cirrhosis or hepatitis.
Saturday, February 03, 2007
Sentry Enzyme Blocks Two Paths To Parkinson's Disease
Source: St. Jude Children's Research Hospital
Date: February 3, 2007
Summary:
The degeneration of brain cells that occurs in Parkinson's disease may be caused by either externally provoked cell death or internally initiated suicide when the molecule that normally prevents these fatal alternatives is missing, according to studies in mouse models by investigators at St. Jude Children's Research Hospital.
Date: February 3, 2007
Summary:
The degeneration of brain cells that occurs in Parkinson's disease may be caused by either externally provoked cell death or internally initiated suicide when the molecule that normally prevents these fatal alternatives is missing, according to studies in mouse models by investigators at St. Jude Children's Research Hospital.
Monday, August 22, 2005
Scientists Find Mechanism for Neural Stem Cell Death
Source: Korea Times
Date: August 22, 2005
Summary:
A team of South Korean scientists has uncovered the mechanism of neural stem cell death, a discovery expected to help treat such degenerative diseases as Parkinson’s and Alzheimer’s.
Date: August 22, 2005
Summary:
A team of South Korean scientists has uncovered the mechanism of neural stem cell death, a discovery expected to help treat such degenerative diseases as Parkinson’s and Alzheimer’s.
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