Links for Keyword: Trophic Factors

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Brain-derived neurotrophic factor (BDNF) has been a subject of keen interest in neuroscientific circles for several years, turning up in studies of conditions ranging from central hypoventilation syndrome to obsessive-compulsive disorder, depression, bipolar disorder and schizophrenia -- a range of disorders uncannily parallel to those produced by mutations in the "Rett gene," MeCP2. In 2003, two groups found that MeCP2 regulates BDNF transcription, but sorting out the complex relationship between the two proteins has been quite challenging. New studies from the labs of Michael Greenberg at Children's Hospital Boston and David Katz at Case Western School of Medicine have begun to shed light on the interplay of MeCP2 and BDNF. Because Rett syndrome (RTT) develops during early childhood, when sensory experiences normally stimulate the development of synaptic circuits, some researchers hypothesized that the fundamental defect in RTT is a failure of synaptic plasticity or maturation. Early support for this hypothesis came from studies showing that MeCP2 expression normally increases as neurons mature. Conversely, RTT patients and mice lacking MeCP2 suffer defects in synaptic plasticity, learning and memory, all of which are dependent on experience – so there is some link between experience and the change in neuronal function it would normally produce that is missing when MeCP2 is not functioning properly. Zhou et al. (Greenberg lab) have found at least part of that missing link. In a paper just published in Neuron, they show that increases in neuronal activity result in phosphorylation of MeCP2 at a particular residue (S421) which, in turn, increases transcription of certain genes, including Bdnf, that are required for experience-dependent brain maturation.

Related chapters from BP7e: Chapter 18: Attention and Higher Cognition; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 13: Memory, Learning, and Development
Link ID: 9512 - Posted: 06.24.2010

But OHSU researcher says jump in BDNF, neurogenesis may not be beneficial PORTLAND, Ore. – Exercise enthusiasts have more reasons to put on their running shoes in the morning, but an Oregon Health & Science University scientist says they shouldn't step up their work-outs just yet. A study published today in the journal Neuroscience, journal of the International Brain Research Organization, confirmed that exercise increases the chemical BDNF – brain-derived neurotrophic factor – in the hippocampus, a curved, elongated ridge in the brain that controls learning and memory. BDNF is involved in protecting and producing neurons in the hippocampus. "When you exercise, it's been shown you release BDNF," said study co-author Justin Rhodes, Ph.D., a postdoctoral fellow in the Department of Behavioral Neuroscience at OHSU's School of Medicine and at the Veterans Administration Medical Center in Portland. "BDNF helps support and strengthen synapses in the brain. We find that exercise increases these good things."

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: 4307 - Posted: 06.24.2010

Results Hold Possibilities For Treating Parkinson’s and Lou Gehrig’s Disease HOUSTON, Jan. 18, 2002 – New research from University of Houston scientists may lead to techniques for jump-starting the faulty "wiring" in damaged nerve cells, and suggests possible avenues for treating spinal cord injuries, Parkinson’s disease and amyotrophic lateral sclerosis, or ALS, also known as Lou Gehrig’s disease. University of Houston scientists studying how spinal nerve cells in chicken embryos develop and function have found that chemicals called growth factors play a key role in regulating how embryonic nerve cells acquire the ability to start processing information. "In some cases, when nerves are damaged or succumb to neurodegenerative diseases such as ALS and Parkinson’s, they don’t die, but they quit working and may actually revert to an immature embryonic-like state," says Stuart Dryer, a neuroscientist in the department of biology and biochemistry at UH.

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: 1397 - Posted: 06.24.2010

St. Louis, – A tiny change in the cells of patients with neurofibromatosis (NF) seems to contribute to formation of aggressive tumors and could help explain why the disease — which predisposes patients to develop tumors — affects people in different ways. Reporting in the January 2002 issue of the American Journal of Human Genetics, investigators at Washington University School of Medicine in St. Louis describe a small, molecular variation in some tumor samples taken from neurofibromatosis patients. “Neurofibromatosis is a common, inherited genetic disease that affects about one in 3,500 people,” says principal investigator Nicholas O. Davidson, M.D., professor of medicine and of molecular biology and pharmacology and director of the Division of Gastroenterology at Washington University School of Medicine. “The gene responsible spans a large region of chromosome 17, but we have found that a very small change in the NF gene’s messenger RNA can inactivate the final product of this gene, a protein called neurofibromin.”

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: 1290 - Posted: 06.24.2010

By Roberta Friedman Scientists know that small variations in certain genes can predispose people to cancers or heart disease. Now researchers are starting to show a direct, quantifiable effect on learning traceable to these types of genetic influences: single-nucleotide polymorphisms. A difference in just one amino acid in a protein might explain why some people learn new motor skills faster and reach higher levels of performance. The protein, called brain-derived neurotro­phic factor (BDNF), is a key driver of synaptic plasti­city, the ability of the connections between brain cells to change in strength. This plasticity is an important factor in learning, explains neurologist Janine Reis, who led the study at the National Institutes of Health. According to Reis, this finding offers the first evidence that slight variations in BDNF’s structure affect learning ability. Volunteers with one type of BDNF learned faster and performed better at a task in which they had to grip a handle more or less tightly to move a computer cursor through a sequence of targets. Those with a different variant never reached the skill level acquired by the faster learners. (The researchers excluded people who play video games.) Other groups have found that the BDNF version that Reis linked with poorer acquisition of skills is associated with reduced function of the hippocampus, a brain region involved in motor learning. © 1996-2009 Scientific American Inc.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 13: Memory, Learning, and Development
Link ID: 12714 - Posted: 06.24.2010

COLUMBUS, Ohio - Researchers here in collaboration with a group in California have discovered that a protein normally thought only to be a component in the immune system actually plays a key role in regulating neurotransmission in the central nervous system -- the CNS -- as well. The protein, tumor necrosis factor alpha, or TNF-alpha, has long been known to be a key player in controlling cell death but this new finding offers new insights into how cells interact within the human nervous system. Understanding this new role of TNF-alpha may provide researchers with possible new approaches to treating illnesses such as dementia, Alzheimer's disease, stroke, epilepsy and spinal cord injury. The report was published in the latest issue of the journal Science.

Related chapters from BP7e: Chapter 18: Attention and Higher Cognition; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 11: Emotions, Aggression, and Stress
Link ID: 1761 - Posted: 03.26.2002

Researchers studying learning disabilities associated with neurofibromatosis type 1, or NF1, have traced the problem to excessive activity of a crucial signaling molecule and have successfully reversed the disabilities in mice by giving them an experimental drug. The findings provide hope that these learning problems may one day be treatable in humans. This study provides the first clear picture of what causes learning impairments in NF1, says study author Alcino J. Silva, Ph.D., of the University of California, Los Angeles (UCLA). NF1 is a genetic disorder that affects about one in every 4000 people. Patients with the disorder have an array of symptoms, including benign tumors called neurofibromas and light brown spots on the skin called café-au-lait spots. About half of the affected individuals have cognitive disabilities, which typically include problems with spatial learning (which affects organization and other abilities) and reading. The study appears in the January 16, 2002, electronic edition of Nature* and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS).

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: 1345 - Posted: 01.17.2002