by Apoorva Mandavilli Nocturnal frontal lobe epilepsy (NFLE), an abnormal and violent sleep-related movement disorder, has recently been linked to mutations in the subunits of nicotinic acetylcholine receptors (NAChR). The mutations themselves do not directly trigger synchronous firing, California researchers suggested today at the annual meeting of the Society for Neuroscience here. Rather, a decrease in calcium potentiation of the receptors appears to allow a sort of neurological "white noise," which normally travels around the cortex in a controlled fashion during quiet sleep, to disseminate broadly across the entire cortex. NFLE is characterized by twisting and jerking movements, and often accompanied by screaming or other vocalizations. The disorder is commonly misdiagnosed as ordinary motor parasomnias, such as night terrors or sleepwalking. Unlike parasomnias, however, the average age of onset is 10-12 years and displays as clusters of short (less than 60 seconds) movements that recur almost every night, sometimes several times a night. In contrast, parasomniac episodes fade with adolescence, occur much less frequently, and last longer than 3 minutes on average. © Elsevier Science Limited 2000

Keyword: Epilepsy; Sleep
Link ID: 1061 - Posted: 11.27.2001

by Dan Ferber If you want people to remember something you tell them, pay them a dollar afterward. That's the conclusion of a study reported here today. Payments after a study session helped subjects recall a list of words a week later. Another study reported at the same session showed that the effects of emotion on memory fade with age and early Alzheimer's disease. Psychologists have known for years that we tend to remember emotionally loaded experiences better than neutral ones, but they don't yet know how we do it. In past studies, researchers had shown that subjects remembered better when they feel bad at the time they were socking away memory. But no one had tested the effects of making the subjects feel good, says Kristy Nielson of Marquette University. Nielson and a colleague had three groups of subjects try to memorize a list of 30 words. After testing them for recall immediately afterward, they sent them on their way. Before they left, however, the researchers praised one group, did nothing for another group, and paid a third group a dollar. © Elsevier Science Limited 2000

Keyword: Learning & Memory
Link ID: 1060 - Posted: 11.27.2001

by Roberta Friedman So many diseases that destroy the aging brain have been linked with clumping proteins, yet the debate over cause and effect continues. Presented here today, recent findings bolster evidence that protein aggregates themselves may not damage nerve cells directly, or produce the clinical signs. The fibers and where they first appear cause the problem, contend researchers at the University of California, who presented a new way to visualize the process microscopically. Although diseases such as Huntington's and Alzheimer's are described collectively as neurodegeneration, some of their dysfunction may be due to the toxic effects of soluble forms of the affected proteins, says Steven Finkbeiner, assistant investigator at the Gladstone Insitute of Neurological Disease at UC San Francisco. They may actually precede the deposition of the protein in the brain as clumps. © Elsevier Science Limited 2000

Keyword: Huntingtons; Genes & Behavior
Link ID: 1059 - Posted: 11.27.2001

by Roberta Friedman Traditional electron microsopy, supercharged with new computer power, is poised to reveal the exact nature of the molecular structure of the nerve synapse. But due to cuts in funding, Jack McMahan says, a generation of trained microscopists is not there to step up to the task. Speaking here to an airplane hangar-sized room filled with neuroscientists, McMahan projected lilac- and gold-tinted pictures of the active zone of the nerve ending, generated by computer from electron micrographs. His images suggest that an intricate structure of already characterized proteins acts to tie synaptic vesicles at the calcium channels, the crucial triggers for the release of nerve cell messages. © Elsevier Science Limited 2000

Keyword: Miscellaneous
Link ID: 1058 - Posted: 11.27.2001

by Roberta Friedman Details presented here about receptors for the quickly acting nerve cell messengers suggest new therapeutic targets, and show how two systems of nerve signals are linked. At a symposium on the emerging knowledge about how inhibitory messages are received by neurons, Stephen Moss described a new role for a couple of previously known proteins, and suggested that they form a link between slow transmission by the catecholamines and the fast inhibitory transmission by GABA. The slowly acting catecholamines such as dopamine and norepinephrine work through a cascade of kinases that either add phosphate molecules to key proteins inside the neuron, or remove them. Unpublished new findings by Moss, who is a pharmacologist at the University College, London, also link these kinases, called PKA and PKC, to the receptor on the neurotransmitter molecule GABA, which is responsible for fast inhibitory transmission as it crosses a synapse. The link occurs via proteins called RACK (receptor for activated C kinase) and AKAP (A-Kinase anchoring protein). © Elsevier Science Limited 2000

Keyword: Miscellaneous
Link ID: 1057 - Posted: 11.27.2001

by Dan Ferber Normal mice can walk across a narrow beam without falling, but mice with ALS symptoms take frequent tumbles. Transplanted human neuron-like cells helped ALS mice keep their motor skills longer than untreated mice. Two types of cell transplants hold off muscle atrophy in mouse models of amyotrophic lateral sclerosis (ALS). These results offer hope that cell transplants could one day be used to treat this devastating and incurable disease, two research groups announced here this week. ALS, also known as Lou Gehrig's disease, causes spinal-cord neurons that communicate with muscles to waste away, leading within five years to muscle weakness, then paralysis and death. Despite the efforts of researchers, there's little physicians can do for ALS patients; the only FDA-approved drug, sriluzole, prolongs life just six months. © Elsevier Science Limited 2000

Keyword: ALS-Lou Gehrig's Disease ; Regeneration
Link ID: 1056 - Posted: 11.27.2001

by Apoorva Mandavilli Several different teams today presented seemingly contradictory results on gender-specific differences in the response to stress. What is clear, however, is that much more research is needed to identify gender-specific differences and clarify the role of sex hormones in fostering them. Exposure to testosterone during gestation and development gives males an edge in learning while under stress, scientists from Rutgers University reported today. At the same time, German researchers point to an anti-stress role for the female hormone estradiol, and suggest women are less susceptible than men to acute stress. "Some of the results seem to be contradictory but they're really not," said Bruce McEwen, professor of neuroendocrinology at Rockefeller University, who moderated the session. The results differ because "depending on the particular situation and hormonal response, the response is different." © Elsevier Science Limited 2000

Keyword: Stress; Hormones & Behavior
Link ID: 1055 - Posted: 11.27.2001

by Dan Ferber New brain-imaging studies have pinpointed a brain region that helps us grasp mirror images and use them to direct our movement, according to results presented here Monday. The results shed light on how the brain makes sense of information from the space around us. Several years ago, doctors identified a subtle new brain defect in certain patients after a stroke. Patients with so-called mirror agnosia can see an object such as a ball in a mirror, recognize it, and identify it. But when asked to grab the ball, they reach toward the virtual object in the mirror and bump into the mirror, or try to reach around it, says Andrew Butler of Emory University School of Medicine. © Elsevier Science Limited 2000

Keyword: Vision; Stroke
Link ID: 1054 - Posted: 11.27.2001

by Apoorva Mandavilli The miracle drug L-dopa, which has been prescribed for Parkinson's disease (PD) patients for more than 30 years, may itself be partly responsible for the cognitive deficits associated with PD, three independent teams of researchers reported today. PD patients are also impaired at "habit" learning, which depends on the basal ganglia, the part of the brain that is affected by the disease. In addition to severe motor problems, scientists have identified PD-associated affective and cognitive defects, which can ultimately lead to a type of dementia. The cognitive aspects are very different from those seen in patients with Alzheimer's disease (AD), however. Rutgers University neuroscientist Mark Gluck and his colleagues developed computational models for brain simulation, which distinguish between PD and AD defects. AD patients with hippocampal damage have no trouble with simple associations between cues but have trouble transferring that knowledge to a novel task, for example. In contrast, PD patients are slow to learn, but once they master the associations, can apply their knowledge in novel situations. © Elsevier Science Limited 2000

Keyword: Parkinsons
Link ID: 1053 - Posted: 11.27.2001

by Dan Ferber Mice that can't make a peptide hormone called oxytocin can't recognize other mice by smell, so they keep on sniffing them. We can recognize a friend across a crowded room by sight, but mouse pals have to get close and start sniffing. New research, presented here today at a session on olfactory memory, has revealed a key brain hormone that helps them file these socially important odors in their memory banks. Larry Young of Emory University stumbled into the olfactory field accidentally when he and his colleagues were studying mice to uncover the neural basis for social disabilities seen in autism. It turned out that a line of mice lacking a small peptide hormone called oxytocin were socially at a loss, just like conference-goers who find a long-lost colleague but realize they have forgotten his name. Or worse. "They absolutely failed to recognize any individuals they'd seen before," Young says. © Elsevier Science Limited 2000

Keyword: Chemical Senses (Smell & Taste)
Link ID: 1052 - Posted: 11.27.2001

by Roberta Friedman Studies of the genes and signal molecules that govern how a fly's eye develops are leading scientists to the first hints of how the brain is wired. Fruit fly investigator Larry Zipursky of the University of California, Los Angeles, showed how alternative splicing of a newly characterized signal molecule may provide the required diversity to guide the complex wiring of the adult brain. The new focus of Zipursky's research is DSCAM, a receptor first identified in Downs syndrome (the abbreviation stands for Down's Syndrome cell adhesion molecule). Fruit flies have the molecule too, and it appears to help developing neurons find their way to target connections. New, preliminary information shows that DSCAM is localized in the nerve processes and not in the cell bodies, in areas of the fly brain relating to learning, smell, and sight. "It's highly expressed at times of targeting," Zipursky says. © Elsevier Science Limited 2000

Keyword: Development of the Brain
Link ID: 1051 - Posted: 11.27.2001

by Roberta Friedman Research presented here is beginning to reveal the molecular signals that guide the assembly of the brain, and that perhaps can be tapped into for making repairs. The glial cells that most neuroscientists have regarded as merely support cells in fact take an active role in building a brain. A primitive type of glial cell serves as the stem cells that actually generate the brain's neurons. Even in adults, these glial cells can form new neurons, scientists are finding. Evidence presented in a symposium supports the idea that the radial glial cells are actually the stem cells that give rise to neurons, and are not just directing their migration passively. Magdalena Götz and colleagues at the Max-Plank Institute of Neurobiology find that a transcription factor, Pax6, is used in the radial glial cells that are forming neurons. © Elsevier Science Limited 2000

Keyword: Glia; Neurogenesis
Link ID: 1050 - Posted: 06.24.2010

by Dan Ferber In the depths of the brain, hundreds of genes direct the workings of billions of neurons, which in turn direct the circuits that make us who we are. While some of those genes have been uncovered, hundreds remain unknown. By dissecting neurons and screening for active genes, new research is starting to reveal how dendrites, the signal-receiving end of neurons, go awry to cause diseases such as Fragile X mental retardation. All brain cells collect signals via the branched extensions called dendrites and pass them on via an axon. But beyond the dozens of types of neurons, the detailed patterns of dendrites are as diverse as the trees in a forest. What's more, dendrite malfunction appears to underlie an array of brain disease or injury, including schizophrenia, autism, traumatic brain injury, and fragile X mental retardation. For example, neurons from the hippocampus of mice with fragile X syndrome have more projections called dendritic spines, and the spines are longer and more immature, says James Eberwine of the University of Pennsylvania. © Elsevier Science Limited 2000

Keyword: Development of the Brain; Genes & Behavior
Link ID: 1049 - Posted: 11.27.2001

by Dan Ferber When subjects lie, the anterior cingulate cortex (top center, yellow) gets to work in the brains of almost all subjects. The images represent the brain seen from the top as if it had been sliced horizontally. Researchers have pinpointed a brain region that goes to work when we tell lies, and several other regions that help us read other people's intentions, according to work presented here today. In each case, the brain science validates a doctrine early philosophers and theorists posited about how we think. Polygraph tests measure physiological signs of anxiety, but they're notoriously unreliable, because liars can be calm and truthtellers can be anxious. To get to the root of lying behavior, Daniel Langleben's team at the University of Pennsylvania used a brain-imaging technique called event-related functional magnetic resonance imaging (fMRI) to find out which regions of the brain became metabolically active when a person lies. © Elsevier Science Limited 2000

Keyword: Stress
Link ID: 1048 - Posted: 11.27.2001

by Apoorva Mandavilli Neural stem cells (NSCs) can alleviate neural degeneration by instructing host cells to regenerate, rather than by maturing into neurons themselves, Harvard neurologist Evan Snyder said today. In mice with Purkinje cell (PC) degeneration, Snyder reports, NSCs may be reconstituting the PC layer either by protecting host cells or by stimulating a more vigorous regenerative response. "We think this may be the donor cells secreting things that change the host," Snyder said. "And this may apply not just to NSCs but to many other types [of stem cells]." In fact, he suggests, the new model may explain some functional results now observed in other stem cell experiments. Snyder and his colleagues transplanted donor NSCs into the cerebella of nervous (nr), Purkinje-cell-deficient (pcd), and lurcher (lc) mice with rapid degeneration of PCs. Transplanted NSCs dispersed broadly, but only a minority of them matured into neurons and glial cells, the researchers say. © Elsevier Science Limited 2000

Keyword: Stem Cells
Link ID: 1047 - Posted: 11.27.2001

by Roberta Friedman Nobel laureate Paul Greengard, addressing a packed hall at this meeting of some 28,000 neuroscientists, detailed the inner cascade of signals within a nerve cell that converges on one tiny protein. Greengard is convinced that drug companies can cash in on what we know about this key signal molecule, dubbed DARPP-32. By intelligently targeting new drugs to interfere at various points in the web of inner messages converging on DARPP-32, new therapeutics could act simply by changing the balance that determines whether DARPP-32 is sporting a phosphate molecule, or not. DARPP-32, a 32-kiloDalton-weight molecule first discovered to respond to the neurotransmitter dopamine, is the end result of some thirty years of work by Greengard (who received the 2000 Nobel Prize in physiology and medicine) and others. Seeking to understand how the arrival of a transmitter molecule such as dopamine across the synapse alters brain cell chemistry, researchers have found that all of the signals generated inside the recipient cell funnel through this one molecule. © Elsevier Science Limited 2000

Keyword: Miscellaneous
Link ID: 1046 - Posted: 11.27.2001

by Apoorva Mandavilli Why do individuals have different emotional responses to the same situation? University of Michigan researchers today report that cortical molecules of the stress system play a critical role in shaping individual differences in emotional reactivity. Specifically, increased expression of the glucocorticoid receptor, previously linked to learning and memory, is associated with increased anxiety, said Huda Akil, co-director of the university's Mental Health Research Institute. Using microarrays, Akil and her colleagues are now trying to identify other genes that are important in emotional response. "The brain is where genes and the environment meet to make us emotionally different," Akil said. Investigating brain circuits therefore has profound implications for understanding emotional behavior, and the causes of vulnerability to depression and anxiety disorders. © Elsevier Science Limited 2000

Keyword: Stress; Genes & Behavior
Link ID: 1045 - Posted: 11.27.2001

by Debra A. Titone Language is so frequently touted as the most ?human? of human capacities that I fear we, as a species, have overlooked that which truly distinguishes us from the rest of the natural world - dream interpretation. Early interpretation focused on the divine and often prophetic quality of dreams, guiding ancient humans to create art, world religions and military campaigns. Following the age of reason, dream interpretation took a back seat to scientific objectivity, and dreams were attributed to such things as indigestion, loud noise and anxiety (but see Freud for a later change of heart). Given this checkered past, it is not surprising that the modern study of dreams and the role of sleep in cognition is controversial. However, as detailed in a recent issue of Science, renewed efforts are enhancing our understanding of the role of dreams in the neural basis of such fundamental cognitive activities as memory consolidation. The dream-based memory consolidation hypothesis involves two main sleep stages, rapid eye movement (REM) and non-REM, which are associated with different patterns of neural activity, dreaming behavior and, when interrupted, deleterious effects on memory. © Elsevier Science Limited 2000

Keyword: Sleep; Learning & Memory
Link ID: 1044 - Posted: 11.27.2001

by Roberta Friedman Modern scans of the living human brain reveal a unique region that registers the inner state of the body. The insula, tucked inside the cortical covering of the brain, generates the uniquely human sense of self. The findings confirm concepts first presented by scholars of the nervous system a hundred years ago, and may give insight into syndromes of chronic pain. In a special lecture, neuroanatomist Arthur Craig of the Barrow Neurological Institute in Phoenix, Arizona, presented classic anatomic tracings, as well as cutting edge PET and fMRI scans, that delineate this insular cortex. An entire set of cerebral connections appears to have evolved in people that uniquely create a sense of self, Craig says. The messages start in the spinal cord, quite routinely. The first clue is found where these spinal inputs arrive at the brain's core, in the thalamus. © Elsevier Science Limited 2000

Keyword: Brain imaging; Attention
Link ID: 1043 - Posted: 11.27.2001

by Apoorva Mandavilli The much-celebrated amyloid vaccine approach in Alzheimer's disease (AD) is unlikely to reverse cognitive deficits in symptomatic patients, University of South Florida (USF) researchers cautioned today. Cognitive performance is indeed restored, if only the researchers wait long enough, countered a second team. The presentations, attended by a veritable who's who in AD research and peppered with questions from rivaling teams, carried on the contentious tradition in the AD community, albeit in an overtly polite manner. In the end, Dale Schenk told BioMedNet News, "the [human] clinical trials will tell." Elan Pharmaceuticals, where Schenk is vice president of discovery research, earlier this year began phase II clinical trials of the vaccine. The USF team has previously shown that APP/PS1 double-transgenic mice vaccinated at 8 months are protected from age-related cognitive impairment, as tested by a radial arm water maze. But at 18 months, immunization did not improve cognitive performance, says David Morgan, director of USF's Alzheimer's Research Laboratory. © Elsevier Science Limited 2000

Keyword: Alzheimers
Link ID: 1042 - Posted: 11.27.2001