Links for Keyword: Apoptosis

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 19 of 19

by Michael Marshall There's a downside to everything. When humans evolved bigger brains, we became the smartest animal alive and were able to colonise the entire planet. But for our minds to expand, a new theory goes, our cells had to become less willing to commit suicide – and that may have made us more prone to cancer. When cells become damaged or just aren't needed, they self-destruct in a process called apoptosis. In developing organisms, apoptosis is just as important as cell growth for generating organs and appendages – it helps "prune" structures to their final form. By getting rid of malfunctioning cells, apoptosis also prevents cells from growing into tumours. "Reduced apoptotic function is well known to be associated with cancer onset," says John McDonald of the Georgia Institute of Technology in Atlanta. McDonald compared skin cells from humans, chimpanzees and macaques and found that, compared to cells from other primates, our cells are reluctant to undergo apoptosis. When exposed to apoptosis-triggering chemicals, human cells responded significantly less than the chimp and macaque cells. Fewer human cells died, and they did not change shape in the ways cells do when preparing to die. In 2009, McDonald found that genes promoting apoptosis are down-regulated – essentially suppressed – in humans, and those turning it off are up-regulated (Medical Hypotheses, doi.org/bgkshp). Genes involved in apoptosis are also known to have changed rapidly during human evolution. The new study adds to the evidence that apoptosis is down-regulated in human cells. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17371 - Posted: 10.16.2012

Researchers have genetically manipulated fruit flies so that the flies produce a human protein that protects against the degeneration of neurons similar to those affected in Parkinson’s disease. The protective protein, called a chaperone, suppresses the toxicity of a -synuclein, a protein associated with Parkinson’s disease in humans. Progressive loss of dopaminergic neurons produces the neurological symptoms of Parkinson’s disease. Chaperone proteins normally aid in proper folding of proteins and are involved in protecting against cellular stresses. The findings were reported in the December 21, 2001, issue of Science by Howard Hughes Medical Institute investigator Nancy M. Bonini and colleagues at the University of Pennsylvania School of Medicine. ©2001 Howard Hughes Medical Institute

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 1203 - Posted: 06.24.2010

Milestones reached in understanding how BCL-2 family members control the apoptotic process By Ricki Lewis Apoptosis is about as complex a cellular choreography as one can imagine. Death signals impinge, chromatin cleaves, mitochondria release cell-destroying contents, and membranes undulate and form blebs, eventually shrink-wrapping the shattered cell into neat packages destined for the innards of a phagocyte. Many research groups are deciphering the cascades of proteins that orchestrate the program. Stanley Korsmeyer, a Howard Hughes Medical Institute researcher at the Dana-Farber Cancer Center in Boston, is one of them. In experiments spanning more than a decade, his group has clarified the roles of certain key proteins that regulate the mitochondrial arm of apoptosis. This issues' Hot Papers1,2 "represent milestones in the research on how BCL-2 family members control the process of cell death," says Luca Scorrano, an assistant scientist at the Dulbecco Telethon Institute at Padova University in Italy and a recent member of the Korsmeyer team. ©2003, The Scientist Inc.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3599 - Posted: 06.24.2010

Cells get survival signals even when the axon cannot internalize large beads By Rabiya S. Tuma The reports of two research groups interested in retrograde signaling caught the attention of investigators at the recent Society for Neuroscience (SFN)meeting; the teams used similar methods but arrived at two distinct conclusions. One team says that there is only one way to send nerve growth factor (NGF) signals from the axon to the cell body. The other group thinks that this retrograde signaling occurs in another way. Previously, scientists thought that when NGF bound to TrkA receptors at the axon tip, the complex was internalized into a vesicle and shipped back up the length of the axon to the cell body, where the complex conveys a signal for survival and growth. But Bronwyn MacInnis and Bob Campenot, Department of Cell Biology, University of Alberta, have caused a minor earthquake in the field of retrograde signaling with their results.1 Many scientists, including David Kaplan of the Research Institute at The Hospital for Sick Children, Toronto, see merit in the new thought process. "Bob's work has changed the paradigm." ©2002, The Scientist Inc.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 3140 - Posted: 06.24.2010

NewScientist.com news service Ground-breaking work on the genetic regulation of organ development and programmed cell death has won three researchers the 2002 Nobel Prize in Medicine. The research led to a new understanding of diseases ranging from cancer to strokes to AIDS. John Sulston of the Sanger Institute, UK, Sydney Brenner, a UK national working at the Molecular Sciences Institute in Berkeley, US and H. Robert Horvitz, at the Massachusetts Institute of Technology in Boston will share the $1 million prize. The trio have "opened possibilities to follow cell division and differentiation from the fertilised egg to the adult" and identified "key genes regulating organ development," the jury said. "The discoveries are important for medical research and have shed new light on the pathogenesis of many diseases." © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 2761 - Posted: 06.24.2010

Copyright © 2002 AP Online By KIM GAMEL, Associated Press STOCKHOLM, Sweden - Two Britons and an American won this year's Nobel Prize in medicine for discoveries concerning how genes regulate organ development and a process of programmed cell suicide. British citizens Sydney Brenner and John E. Sulston and American H. Robert Horvitz shared the prize, worth about $1 million. Brenner, of the Molecular Sciences Institute in Berkeley, Calif., and Sulston, of the Sanger Center at England's Cambridge University will split the prize with Horvitz, of the Massachusetts Institute of Technology. Copyright © 2001 Nando Media

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 2756 - Posted: 06.24.2010

Two different routes find the mammalian enemies of apoptosis inhibitors By Laura DeFrancesco Apoptosis, or programmed cell death, provides organisms a way to remove unwanted cells, such as during morphogenesis, or to defend against viral infection. Of course, certain molecules exist to prohibit apoptosis. One of these proteins, aptly named Inhibitor of Apoptosis Protein (IAP), was first found in viruses, which use them to keep host cells alive while the virus replicates and propagates. These IAPs interfere with key effectors of apoptosis, the family of proteases known as caspases, which, when activated, literally digest the cell from the inside out. But the story doesn't end there: antagonists exist to antagonize the IAPs; these molecules send the cell back down the apoptosis pathway. For example, three IAP antagonists, Reaper, Grim and HID, have been identified in Drosophila. These proteins promote cell death by binding to the IAPs, keeping them from suppressing caspase activity. However, no similar IAP antagonists had been identified in mammals until the labs of David Vaux, Xiaodong Wang, and the editors of Cell crossed paths. C. Du et al., "Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition," Cell, 102:33-42, July 7, 2000. The Scientist 16[5]:29, Mar. 4, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 1614 - Posted: 06.24.2010

CHAMPAIGN, Ill. -- A protein known primarily for its role in killing cells also plays a part in memory formation, researchers at the University of Illinois at Urbana-Champaign report. Their work exploring how zebra finches learn songs could have implications for treatment of neurodegenerative conditions such as dementia and Alzheimer's disease. When activated, the enzyme caspase-3 triggers a synaptic process essential for memory storage, according to Graham R. Huesmann and David F. Clayton of the department of cell and developmental biology and of the U. of I. Beckman Institute for Advanced Science and Technology. Their article, which appears in the Dec. 21 issue of the journal Neuron, describes their findings, which provide "the first direct evidence of a change in the availability of activated caspase-3 protein in the brain during the process of memory formation." Caspase-3 is best known for its role in a biochemical cascade that leads to apoptotic cell death. These new findings demonstrate that the enzyme acts differently under different conditions, and suggest that its regulation in the brain is more complex than previously thought. Huesmann and Clayton examined the brains of zebra finches after exposing the birds to tape recordings of the songs of other birds. They found an increase in the concentration of activated caspase-3 in post-synaptic sites of the auditory forebrain shortly after the birds were exposed to unfamiliar bird songs. Exposure to familiar songs caused no significant increase in the enzyme.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 14: Attention and Consciousness
Link ID: 9783 - Posted: 12.22.2006

LA JOLLA, CA - Wiring the developing brain is like creating a topiary garden. Shrubs don't automatically assume the shape of ornamental elephants, and neither do immature nerve cells immediately recognize the "right" target cell. Abundant foliage, either vegetal or neuronal, must first sprout and then be sculpted into an ordered structure. Neurons extend fibers called axons to target cells in an exuberant manner--some branch to the "wrong" cells while others shoot past their target cells. Axon pieces that went astray degenerate, effectively being "pruned" back. Similarly, when axons are forcibly severed or seriously injured by disease in adults, they die and are removed by degeneration. Scientists have speculated that the same molecular shears used to trim axon branches in injured adult axons also do so during normal developmental pruning. In a forthcoming issue of Neuron, teams at the Salk Institute for Biological Studies and Stanford University revise that notion and, in doing so, suggest how nerve function could be preserved after injury. The collaboration began when senior co-authors Liqun Luo, PhD., a professor at Stanford University and Howard Hughes Medical Investigator, and Dennis D.M. O'Leary, a professor in the Salk Molecular Neurobiology Laboratory, co-wrote a review on neurodegeneration. Of O'Leary, Luo says, "When they asked me to write this review I found that half these things were started by Dennis." O'Leary adds, "We had a great time writing the review and it hatched the idea to combine our ideas."

Related chapters from BP7e: Chapter 19: Language and Hemispheric Asymmetry; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Our Divided Brain; Chapter 13: Memory, Learning, and Development
Link ID: 9037 - Posted: 06.15.2006

Background. The hippocampal formation has long been associated with the execution of higher-order cognitive functions, and impairment of this structure following severe stress and aging has been linked to cognitive disturbances. In order to understand the involvement of the hippocampal formation in the mediation of normal and pathological behaviors, much attention has recently been devoted to hippocampal neurogenesis. The dentate gyrus of the hippocampal formation has the ability to generate new neurons throughout the entire life. Surviving de novo produced cells develop into granule neurons and integrate into the functional circuitry. Neurogenesis has been proposed to play a role in hippocampal-mediated learning and has been implicated in the appearance of behavioral pathologies associated with the hippocampal formation. Aim of the work. Although evidence suggest that neurogenesis play a role in spatial learning, the effect of learning on cell proliferation remains unclear. The authors generated and tested the hypothesis that different phases of spatial learning measured in the Morris water maze have distinct actions on cell proliferation. In this task, two phases of learning can be distinguished: an early phase during which performance improves rapidly, and a late phase during which asymptotic levels of performance are reached. These two phases seem to involve different brain processes and consequently may differentially influence neurogenesis.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 4608 - Posted: 11.27.2003

In a study conducted in rats, scientists have determined that drugs that block the action of a group of DNA-repair enzymes can protect brain cells from damage triggered by an overdose of insulin. If these drugs are shown to produce the same effect in humans, they could become the first tool available for prevention of brain damage that can result from hypoglycemic shock, also known as insulin shock, in patients with diabetes. The study was conducted by scientists at the San Francisco Veterans Affairs Medical Center (SFVAMC) and appears in the November 19 issue of the Journal of Neuroscience. The drugs, PARP inhibitors, have already been shown to protect human heart and brain cells from damage following heart attack and stroke, and are currently approved for testing in phase-2 clinical trials for victims of heart attack. "Every hospital emergency department sees one or more cases of hypoglycemic coma each year," says Raymond Swanson, MD, chief of Neurology Service at SFVAMC and a professor in the Department of Neurology, University of California, San Francisco (UCSF.) "Up to this point, we don't have any way to treat these patients except to give them glucose, which pulls them out of insulin shock, but doesn't do anything to stop the cell death process that is triggered by severe hypoglycemia. PARP inhibitors rescue neurons [brain cells] which would otherwise go on to die even though blood glucose is restored."

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 4574 - Posted: 11.21.2003

GAINESVILLE, Fla. --- Trimming the waistline may not be the only reason to cut calories after the New Year: Doing so also may protect the brain from aging. In the first study to look specifically at the effects of life-long calorie-restricted diets on brain cells, University of Florida researchers determined certain proteins linked to cell death that naturally increase with age were significantly reduced in the brains of rats whose calories were limited. More important, they found the levels of a beneficial protein known to provide potent protection against neuron death were twice as high in older rats whose calories were restricted by 40 percent.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 3278 - Posted: 01.10.2003

Oxidative stress is implicated in a fast-growing list of human conditions, from the superficial (e.g., wrinkled skin) to the deadly: diseases such as cancer, heart disease and neurodegenerative disorders including Lou Gehrig's disease (amyotrophic lateral sclerosis or ALS). Researchers at The Jackson Laboratory announced that they have located a gene that protects certain brain and retinal neurons from oxidative stress, and prevents neurodegeneration. Many normal metabolic functions produce free radicals--highly unstable forms of oxygen. Despite their notoriety, these molecules in fact have several beneficial roles, such as helping white blood cells attack bacteria, viruses and virus-damaged cells. Oxidative stress occurs when the amount of free radicals exceeds the normal antioxidant capacity of a cell, leading to cell damage.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 5: The Sensorimotor System
Link ID: 2711 - Posted: 09.26.2002

Writing in the July 12 issue of the journal Science, Hopkins-led researchers say they have identified in neurons a novel form of "programmed" cell death unlike those already known -- apoptosis and necrosis. The finding, in mouse cells, defines for the first time a window of opportunity to prevent a neuron's death and perhaps find new targets to try to treat Parkinson disease, stroke and traumatic brain injury, says Valina Dawson, Ph.D., of Hopkins' Institute for Cell Engineering and professor of neuroscience at the Johns Hopkins School of Medicine. "All cell death is 'programmed' in that it results from a particular series of events," says Dawson. "But up to a certain point, the outcome is not inevitable and interference with the process can prevent or delay cell death. Knowing when that window of opportunity closes is critical."

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 2320 - Posted: 07.17.2002

Points to Need for Blood Sugar Control in Diabetic and Obese Women Boston--March, 2002--Diabetic mothers could have a surprising culprit to blame for their high risk of having babies with neural tube defects. Scientists at Joslin Diabetes Center working with mice report in the March 15 Genes and Development that a protein normally involved in programmed cell death may, as a consequence of high blood sugar levels, mistakenly tell the cells of the early developing neural tube to die. It is not clear whether the protein, p53, plays a similar role in human neural tube defects, which include spina bifida (where the spinal cord is not completely enclosed) and exencephaly (where the brain is exposed and the skull is not fully formed). But the report provides a possible explanation for a class defects that appears to be on the rise. Even with good control of diabetes, the risk for neural tube and other birth defects is two to five times higher than normal if a mother has diabetes. That risk could increase as diabetes and obesity, both of which can cause high blood sugar, makes inroads into younger populations. "I think there is a very large population of women at risk for having a baby with a neural tube defect who are not being looked at aggressively because they have not been diagnosed as having diabetes, and yet, their blood glucose may be higher than normal" said Mary Loeken, PhD, who is a researcher at Joslin and assistant professor of medicine (physiology) at Harvard Medical School.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 1749 - Posted: 03.24.2002

Rockefeller Scientist discovers molecular messengers that rescue cells from death A developing cell in the human body sits on the edge of death. Proteins called Grim, Reaper and Hid stand poised, ready to unleash other toxic proteins. Only if a protein messenger from another cell arrives in time to call off the killing, will the cell then mature into any one of the various types of body cells, such as skin, liver and brain. But how these protein messengers command cells to survive has remained a mystery until now. For the first time, the entire team of molecular messengers responsible for issuing certain brain cells with orders to survive has been identified by a Rockefeller University scientist and his colleagues. They report their results in the Feb 1 issue of Developmental Cell.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 1461 - Posted: 02.02.2002

By David F. Salisbury Critical new data on a complex enzyme that lies at the crossroad between cell suicide and tumor suppression has opened a promising new front in the battle to find effective treatments for stroke and cancer. Scientists at Vanderbilt University and Northwestern University have determined the three-dimensional structure of a critical region of Death Associated Protein Kinase (DAPK) and created a quantitative assay capable of measuring its activity.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 15: Language and Our Divided Brain
Link ID: 1137 - Posted: 12.08.2001

by Dan Ferber It's no secret that sex hormones mess with the mind and alter behavior, and researchers have known, too, that they alter the shape of specific brain cells. But despite the logical connection, researchers have struggled to prove that the two effects are linked. Janis Weeks' team has shown precisely how steroid hormones affect individual neurons in a caterpillar with a simple nervous system, causing profound changes that help the caterpillar become a moth. The results, presented here in a special lecture, reveal how steroid hormones might affect other animal brains, including our own. Weeks and her colleagues at the University of Oregon study the simple nervous system of a caterpillar called the tobacco hornworm that has a body the length of a human hand. Like other caterpillars, it transforms into a pupa and then an adult moth, and entomologists have long known that a steroid hormone called 20-hydroxyecdysone (20E) triggers each step of the metamorphosis. © Elsevier Science Limited 2000

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 1062 - Posted: 11.27.2001

by Kirsten C. Sadler Recent studies indicate that during apoptosis engulfing cells do not simply dispose of suicidal cells but actively participate in killing them. Even more striking is the observation that a small percentage of target cells may show some morphological signs of apoptosis but then apparently change their mind and return from the brink of death. Once a cell has received a death signal and makes the molecular decision to commit suicide, the killing is carried out in a stepwise fashion by, in most but not all cases, members of the Bcl-2 family, release of cytochrome c and other factors from the mitochondria and, in all cases, activation of the caspase family of proteases. Caspases dismantle the cell and also activate other proteases to aid in the execution. Once the deed is done, the dead cell's neighbors engulf the cell corpse. Some cells return from the brink of death. © Elsevier Science Limited 2000

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 1041 - Posted: 11.27.2001