Posts tagged neuroscience
Articles and news from the latest research reports.
Scientists from the University of Southampton have identified the molecular system that contributes to the harmful inflammatory reaction in the brain during neurodegenerative diseases.
An important aspect of chronic neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, Huntington’s or prion disease, is the generation of an innate inflammatory reaction within the brain.
Results from the study open new avenues for the regulation of the inflammatory reaction and provide new insights into the understanding of the biology of microglial cells, which play a leading role in the development and maintenance of this reaction.
Dr Diego Gomez-Nicola, from the CNS Inflammation group at the University of Southampton and lead author of the paper, says: “The understanding of microglial biology during neurodegenerative diseases is crucial for the development of potential therapeutic approaches to control the harmful inflammatory reaction. These potential interventions could modify or arrest neurodegenerative diseases like Alzheimer disease.
“The future potential outcomes of this line of research would be rapidly translated into the clinics of neuropathology, and would improve the quality of life of patients with these diseases.”
Microglial cells multiply during different neurodegenerative conditions, although little is known about to what extent this accounts for the expansion of the microglial population during the development of the disease or how it is regulated.
Writing in The Journal of Neuroscience, scientists from the University of Southampton describe how they used a laboratory model of neurodegeneration (murine prion disease), to understand the brain’s response to microglial proliferation and dissected the molecules regulating this process. They found that signalling through a receptor called CSF1R is a key for the expansion of the microglial population and therefore drugs could target this.
Dr Diego Gomez-Nicola adds: “We have been able to identify that this molecular system is active in human Alzheimer’s disease and variant Creutzfeldt–Jakob disease, pointing to this mechanism being universal for controlling microglial proliferation during neurodegeneration. By means of targeting CSF1R with selective inhibitors we have been able to delay the clinical symptoms of experimental prion disease, also preventing the loss of neurons.”
Cooling may prevent trauma-induced epilepsy
In the weeks, months and years after a severe head injury, patients often experience epileptic seizures that are difficult to control. A new study in rats suggests that gently cooling the brain after injury may prevent these seizures.
“Traumatic head injury is the leading cause of acquired epilepsy in young adults, and in many cases the seizures can’t be controlled with medication,” says senior author Matthew Smyth, MD, associate professor of neurological surgery and of pediatrics at Washington University School of Medicine in St. Louis. “If we can confirm cooling’s effectiveness in human trials, this approach may give us a safe and relatively simple way to prevent epilepsy in these patients.”
The researchers reported their findings in Annals of Neurology.
Cooling the brain to protect it from injury is not a new concept. Cooling slows down the metabolic activity of nerve cells, and scientists think this may make it easier for brain cells to survive the stresses of an injury.
Doctors currently cool infants whose brains may have had inadequate access to blood or oxygen during birth. They also cool some heart attack patients to reduce peripheral brain damage when the heart stops beating.
Smyth has been exploring the possibility of using cooling to prevent seizures or reduce their severity.
“Warmer brain cells seem to be more electrically active, and that may increase the likelihood of abnormal electrical discharges that can coalesce to form a seizure,” Smyth says. “Cooling should have the opposite effect.”
Smyth and colleagues at the University of Washington and the University of Minnesota test potential therapies in a rat model of brain injury. These rats develop chronic seizures weeks after the injury.
Researchers devised a headset that cools the rat brain. They were originally testing its ability to stop seizures when they noticed that cooling seemed to be not only stopping but also preventing seizures.
Scientists redesigned the study to focus on prevention. Under the new protocols, they put headsets on some of the rats that cooled their brains by less than 4 degrees Fahrenheit. Another group of rats wore headsets that did nothing. Scientists who were unaware of which rats they were observing monitored them for seizures during treatment and after the headsets were removed.
Rats that wore the inactive headset had progressively longer and more severe seizures weeks after the injury, but rats whose brains had been cooled only experienced a few very brief seizures as long as four months after injury.
Brain injury also tends to reduce cell activity at the site of the trauma, but the cooling headsets restored the normal activity levels of these cells.
The study is the first to reduce injury-related seizures without drugs, according to Smyth, who is director of the Pediatric Epilepsy Surgery program at St. Louis Children’s Hospital.
“Our results show that the brain changes that cause this type of epilepsy happen in the days and weeks after injury, not at the moment of injury or when the symptoms of epilepsy begin,” says Smyth. “If clinical trials confirm that cooling has similar effects in humans, it could change the way we treat patients with head injuries, and for the first time reduce the chance of developing epilepsy after brain injury.”
Smyth and his colleagues have been testing cooling devices in humans in the operating room, and are planning a multi-institutional trial of an implanted focal brain cooling device to evaluate the efficacy of cooling on established seizures.
Clues to Fetal Alcohol Risk: Molecular switch promises new targets for diagnosis and therapy
Fetal alcohol syndrome is the leading preventable cause of developmental disorders in developed countries. And fetal alcohol spectrum disorder (FASD), a range of alcohol-related birth defects that includes fetal alcohol syndrome, is thought to affect as many as 1 in 100 children born in the United States.
Any amount of alcohol consumed by the mother during pregnancy poses a risk of FASD, a condition that can include the distinct pattern of facial features and growth retardation associated with fetal alcohol syndrome as well as intellectual disabilities, speech and language delays, and poor social skills. But drinking can have radically different outcomes for different women and their babies. While twin studies have suggested a genetic component to susceptibility to FASD, researchers have had little success identifying who is at greatest risk or what genes are at play.
Research from Harvard Medical School and Veterans Affairs Boston Healthcare System sheds new light on this question, identifying for the first time a signaling pathway that might determine genetic susceptibility for the development of FASD. The study was published online Feb. 19 in the journal Proceedings of the National Academy of Sciences.
“Our work points to candidate genes for FASD susceptibility and identifies a path for the rational development of drugs that prevent ethanol neurotoxicity,” said Michael Charness, chief of staff at VA Boston Healthcare System and HMS professor of neurology. “And importantly, identifying those mothers whose fetuses are most at risk could help providers better target intensive efforts at reducing drinking during pregnancy.”
The discovery also solves a riddle that had intrigued Charness and other researchers for nearly two decades. In 1996, Charness and colleagues discovered that alcohol disrupted the work of a human protein critical to fetal neural development—a major clue to the biological processes of FASD. The protein, L1, projects through the surface of a cell to help it adhere to its neighbors. When Charness and his team introduced the protein to a culture of mouse fibroblasts cells, L1 increased cell adhesion. Tellingly, the effect was erased in the presence of ethanol (beverage alcohol).
Charness and his team went on to develop multiple cell lines from that first culture, and that’s where they encountered the riddle: In some of those lines, alcohol disrupted L1’s adhesive effect, while in others it did not.
“How could it be possible that a cell that expresses L1 is completely sensitive to alcohol, and others that express it are completely insensitive?” asked Charness, who is also faculty associate dean for veterans hospital programs at HMS and assistant dean at Boston University School of Medicine.
Clearly, something else was affecting the protein’s sensitivity to alcohol — but what? Studies of twins provided one clue: Identical twins are more likely than fraternal twins to have the same diagnosis, positive or negative, for FASD. “That concordance suggests that there are modifying genes, susceptibility genes, that predispose to this condition,” Charness said.
First signals from brain nerve cells with ultrathin nanowires
Electrodes operated into the brain are today used in research and to treat diseases such as Parkinson’s. However, their use has been limited by their size. At Lund University in Sweden, researchers have, for the first time, succeeded in implanting an ultrathin nanowire-based electrode and capturing signals from the nerve cells in the brain of a laboratory animal.
The researchers work at Lund University’s Neuronano Research Centre in an interdisciplinary collaboration between experts in subjects including neurophysiology, biomaterials, electrical measurements and nanotechnology. Their electrode is composed of a group of nanowires, each of which measures only 200 nanometres (billionths of a metre) in diameter.
Such thin electrodes have previously only been used in experiments with cell cultures.
“Carrying out experiments on a living animal is much more difficult. We are pleased that we have succeeded in developing a functioning nano-electrode, getting it into place and capturing signals from nerve cells”, says Professor Jens Schouenborg, who is head of the Neuronano Research Centre.
He sees this as a real breakthrough, but also as only a step on the way. The research group has already worked for several years to develop electrodes that are thin and flexible enough not to disturb the brain tissue, and with material that does not irritate the cells nearby. They now have the first evidence that it is possible to obtain useful nerve signals from nanometre-sized electrodes.
The research will now take a number of directions. The researchers want to try and reduce the size of the base to which the nanowires are attached, improve the connection between the electrode and the electronics that receive the signals from the nerve cells, and experiment with the surface structure of the electrodes to see what produces the best signals without damaging the brain cells.
“In the future, we hope to be able to make electrodes with nanostructured surfaces that are adapted to the various parts of the nerve cells – parts that are no bigger than a few billionths of a metre. Then we could tailor-make each electrode based on where it is going to be placed and what signals it is to capture or emit”, says Jens Schouenborg.
When an electrode is inserted into the brain of a patient or a laboratory animal, it is generally anchored to the skull. This means that it doesn’t move smoothly with the brain, which floats inside the skull, but rather rubs against the surrounding tissue, which in the long term causes the signals to deteriorate. The Lund group’s electrodes will instead be anchored by their surface structure.
“With the right pattern on the surface, they will stay in place yet still move with the body – and the brain – thereby opening up for long-term monitoring of neurones”, explains Jens Schouenborg.
He praises the collaboration between medics, physicists and others at the Neuronano Research Centre, and mentions physicist Dmitry B. Suyatin in particular. He is the principal author of the article which the researchers have now published in the international journal PLOS ONE.
The overall goal of the Neuronano Research Centre is to develop electrodes that can be inserted into the brain to study learning, pain and other mechanisms, and, in the long term, to treat conditions such as chronic pain, depression and Parkinson’s disease.
(Source: lunduniversity.lu.se)
Bilingual children have a better “working memory” than monolingual children
A study conducted at the University of Granada and the University of York in Toronto, Canada, has revealed that bilingual children develop a better working memory –which holds, processes and updates information over short periods of time– than monolingual children. The working memory plays a major role in the execution of a wide range of activities, such as mental calculation (since we have to remember numbers and operate with them) or reading comprehension (given that it requires associating the successive concepts in a text).
The objective of this study –which was published in the last issue of the Journal of Experimental Child Psychology– was examining how multilingualism influences the development of the “working memory” and investigating the association between the working memory and the cognitive superiority of bilingual people found in previous studies.
Executive Functions
The working memory includes the structures and processes associated with the storage and processing of information over short periods of time. It is one of the components of the so-called “executive functions”: a set of mechanisms involved in the planning and self-regulation of human behavior. Although the working memory is developed in the first years of life, it can be trained and improved with experience.
According to the principal investigator of this study, Julia Morales Castillo, of the Department of Experimental Psychology of the University of Granada, this study contributes to better understand cognitive development in bilingual and monolingual children. “Other studies have demonstrated that bilingual children are better at planning and cognitive control (i.e. tasks involving ignoring irrelevant information or requiring a dominant response). But, to date, there was no evidence on the influence of bilingualism on the working memory.
The study sample included bilingual children between 5 and 7 years of age (a critical period in the development of the working memory). The researchers found that bilingual children performed better than monolingual children in working memory tasks. Indeed, the more complex the tasks the better their performance. “The results of this study suggest that bilingualism does not only improve the working memory in an isolated way, but they affect the global development of executive functions, especially when they have to interact with each other”, Morales Castillo states.
Music Education
According to the researcher, the results of this study “contribute to the growing number of studies on the role of experience in cognitive development”. Other studies have demonstrated that children performing activities such as music education have better cognitive capacities. “However, we cannot determine to what extent children perform these activities due to other factors such as talent or personal interest”.
“However, the children in our study were bilingual because of family reasons rather than because of an interest in languages.
Children With Brain Lesions Able To Use Gestures Important To Language Learning
Children with brain lesions suffered before or around the time of birth are able to use gestures – an important aspect of the language learning process– to convey simple sentences, a Georgia State University researcher has found.
Şeyda Özçalışkan, assistant professor of psychology, and fellow researchers at the University of Chicago, looked at children who suffered lesions to one side of the brain to see whether they used gestures similar to typically developing children. She examined gestures such as pointing to a cookie while saying “eat” to convey the meaning “eat cookie,” several months before expressing such sentences exclusively in speech.
“We do know that children with brain injuries show an amazing amount of plasticity (the ability to change) for language learning if they acquire lesions early in life,” Özçalışkan said. “However, we did not know whether this plasticity was characterized by the same developmental trajectory shown for typically developing children, with gesture leading the way into speech. We looked at the onset of different sentence constructions in children with early brain injuries, and wanted to find out if we could see precursors of different sentence types in gesture.
“For children with brain injuries, we found that this pattern holds, similar to typically developing children,” she said. “Children with unilateral brain injuries produce different kinds of simple sentences several months later than typically developing children. More important, the delays we observe in producing different sentences in speech are preceded by a similar delay in producing the same sentences in gesture-speech combinations.”
Children with brain injuries also had a more difficult time in producing complex sentences across gesture and speech, such as conveying relationships between actions, for example saying “help me do it” while making a painting gesture.
“This in turn was later reflected in a much narrower range of complex sentence types expressed in their speech,” Özçalışkan said. “This suggested to us, in general, that producing sentences across gesture and speech may serve as an embodied sensorimotor experience, that might help children take the next developmental step in producing these sentences in speech.
“And if you bypass the gesture-speech combination stage, that might negatively affect developing a broader representation of complex sentence types in speech.”
The researchers also compared children with smaller brain lesions against children with large lesions, and found more of a delay in producing sentences, both in speech and in gesture-speech combinations, in children with large lesions.
The research has implications for developing interventions to help children with the language learning process, “as it shows that gestures are integral to the process of language learning even when that learning is taking place in an injured brain,” Özçalışkan said.
“When children do different kinds of sentence combinations across gesture and speech, that’s like a signal to the caregiver that ‘I’m ready for this,’” she said. “The caregiver can then provide relevant input to the child, and that could in turn help the child take the next developmental step in producing that sentence entirely in speech.”
Genome-wide imaging study identifies new gene associated with Alzheimer’s plaques
A study combining genetic data with brain imaging, designed to identify genes associated with the amyloid plaque deposits found in Alzheimer’s disease patients, has not only identified the APOE gene — long associated with development of Alzheimer’s — but has uncovered an association with a second gene, called BCHE.
A national research team, led by scientists at the Indiana University School of Medicine, reported the results of the study in an article in Molecular Psychiatry posted online Tuesday. The study is believed to be the first genome-wide association study of plaque deposits using a specialized PET scan tracer that binds to amyloid.
The research also is believed to be the first to implicate variations in the BCHE gene in plaque deposits visualized in living individuals who have been diagnosed with Alzheimer’s disease or are at-risk for developing the disease. The enzyme coded by the BCHE gene has previously been studied in post-mortem brain tissue and is known to be found in plaques.
“The findings could recharge research efforts studying the molecular pathways contributing to amyloid deposits in the brain as Alzheimer’s disease develops and affects learning and memory,” said Vijay K. Ramanan, the paper’s first author and an M.D./Ph.D. student at the IU School of Medicine.
The BCHE gene finding “brings together two of the major hypotheses about the development of Alzheimer’s disease,” said Andrew J. Saykin, Psy.D., Raymond C. Beeler Professor of Radiology and Imaging Sciences at IU and principal investigator for the genetics core of the Alzheimer’s Disease Neuroimaging Initiative.
Scientists have long pointed to the loss of an important brain neurotransmitter, acetylcholine, which is depleted early in the development of the disease, as a key aspect of the loss of memory related neurons. The BCHE gene is responsible for an enzyme that breaks down acetylcholine in the brain. The other major Alzheimer’s hypothesis holds that the development of the amyloid plaques is the primary cause of the disease’s debilitating symptoms. As it turns out, the enzyme for which the BCHE gene codes is also found in significant quantities in those plaques.
“This study is connecting two of the biggest Alzheimer’s dots,” said Dr. Saykin, director of the Indiana Alzheimer Disease Center and the IU Center for Neuroimaging at the IU Health Neuroscience Center.
“The finding that BCHE gene variant predicts the extent of plaque deposit in PET scans among people at risk for Alzheimer’s disease is likely to reinvigorate research into drugs that could modify the disease by affecting the BCHE enzyme or its metabolic pathway,” he said. Some existing drugs inhibit this enzyme, but it is unclear whether this influences plaque deposits.
Overall, the results appear to offer scientists new potential targets for drugs to slow, reverse or even prevent the disease. Alzheimer’s disease affects an estimated 5.4 million Americans and has proven resistant to treatments that do more than temporarily slow the worsening of symptoms.
Amyloid plaque deposits build up abnormally in the brains of Alzheimer’s patients and are believed to play an important role in the memory loss and other problems that plague patients.
The study makes use of an imaging agent, florbetapir, now approved for use by the U.S. Food and Drug Administration, that allows physicians to see the level of plaque buildup in a patient’s brain, something that previously could be determined only with an autopsy.
In a genome-wide association study, researchers evaluate alternate versions of many genes to determine whether particular genetic variants are associated with a particular trait — in this case, the amounts of amyloid plaque deposits that the PET scans revealed in the brains of study participants.
Using the imaging agent that enables detection of the plaques in the brain, the researchers conducted PET scans of 555 participants in the Alzheimer’s Disease Neuroimaging Initiative, a long-term public-private research project that includes people at risk for Alzheimer’s disease and patients who have been diagnosed with the disease as well as participants with no symptoms.
With sophisticated statistical analyses, the imaging data was combined with analyses of DNA collected from the 555 participants to determine whether particular gene variants were found more often among patients with higher levels of plaque deposits.
The analysis found that a variant in BCHE was significantly associated with the levels of plaque deposits. As would be expected, the analysis also found a strong association with variants of another gene, APOE, that has long been known to be associated with the development of Alzheimer’s. The effect of BCHE was independent of APOE, however. Moreover, the effects of the two genes were additive — that is, people with the suspect variants of both genes had more plaque deposits than people who had only one of the variants associated with plaque development.
Omega-3 Lipid Emulsions Markedly Protect Brain After Stroke in Mouse Study
Triglyceride lipid emulsions rich in an omega-3 fatty acid injected within a few hours of an ischemic stroke can decrease the amount of damaged brain tissue by 50 percent or more in mice, reports a new study by researchers at Columbia University Medical Center.
The results suggest that the emulsions may be able to reduce some of the long-term neurological and behavioral problems seen in human survivors of neonatal stroke and possibly of adult stroke, as well. The findings were published today in the journal PLoS One.
Currently, clot-busting tPA (recombinant tissue-type plasminogen activator) is the only treatment shown to improve recovery from ischemic stroke. If administered soon after stroke onset, the drug can restore blood flow to the brain but may not prevent injured, but potentially salvageable, neurons from dying.
Drugs with neuroprotective qualities that can prevent the death of brain cells damaged by stroke are needed, but even after 30 years of research and more than 1000 agents tested in animals, no neuroprotectant has been found effective in people.
Omega-3 fatty acids may have more potential as neuroprotectants because they affect multiple biochemical processes in the brain that are disturbed by stroke, said the study’s senior author, Richard Deckelbaum, MD, director of the Institute of Human Nutrition at Columbia’s College of Physicians & Surgeons. “The findings also may be applicable to other causes of ischemic brain injury in newborns and adults,” added co-investigator Vadim S. Ten, MD, PhD, an associate professor of pediatrics from the Department of Pediatrics at Columbia.
The effects of the omega-3 fatty acids include increasing the production of natural neuroprotectants in the brain, reducing inflammation and cell death, and activating genes that may protect brain cells. Omega-3 fatty acids also markedly reduce the release of harmful oxidants into the brain after stroke. “In most clinical trials in the past, the compounds tested affected only one pathway. Omega-3 fatty acids, in contrast, are very bioactive molecules that target multiple mechanisms involved in brain death after stroke,” Dr. Deckelbaum said.
The study revealed that an emulsion containing only DHA (docosahexaenoic acid), but not EPA (eicosapentaenoic acid), in a triglyceride molecule reduced the area of dead brain tissue by about 50 percent or more even when administered up to two hours after the stroke. Dr. Deckelbaum noted, “Since mice have a much faster metabolism than humans, longer windows of time for therapeutic effect after stroke are likely in humans.” Eight weeks after the stroke, much of the “saved” mouse brain tissue was still healthy, and no toxic effects were detected.
(Image: Shutterstock)
Fragile X makes brain cells talk too much
The most common inherited form of mental retardation and autism, fragile X syndrome, turns some brain cells into chatterboxes, scientists at Washington University School of Medicine in St. Louis report.
The extra talk may make it harder for brain cells to identify and attend to important signals, potentially establishing an intriguing parallel at the cellular level to the attention problems seen in autism.
According to the researchers, understanding the effects of this altered signaling will be important to developing successful treatments for fragile X and autism.
“We don’t know precisely how information is encoded in the brain, but we presume that some signals are important and some are noise,” says senior author Vitaly Klyachko, PhD, assistant professor of cell biology and physiology. “Our theoretical model suggests that the changes we detected may make it much more difficult for brain cells to distinguish the important signals from the noise.”
The findings appear Feb. 20 in Neuron.
Fragile X is caused by mutations in a gene called Fmr1. This gene is found on the X chromosome, one of the two sex chromosomes. Females have two copies of that chromosome, while males only have one. As a result, males have fragile X syndrome more often than females, and the effects in males tend to be more severe.
Symptoms of fragile X include mental retardation, hyperactivity, epilepsy, impulsive behavior, and delays in the development of speech and walking. Fragile X also affects anatomy, leading to unusually large heads, flat feet, large body size and distinctive facial features. Thirty percent of fragile X patients are autistic.
Scientists deleted the Fmr1 gene many years ago in mice to create a model of fragile X. Without Fmr1, the mice have abnormalities in brain cells and social and behavioral deficits similar to those seen in human fragile X.
According to Klyachko, nearly all fragile X mouse studies in the past two decades have focused on how Fmr1 loss affects dendrites, the branches of nerve cells that receive signals. In contrast, his new study finds significant changes in axons, the branches of nerve cells that send signals.
Normally, signals travel down the axon as surges of electrical energy. These surges only last for tiny fractions of a second, briefly causing the axon to release compounds known as neurotransmitters into the short gap between nerve cells. The neurotransmitters cross the gap and bind to their receptors on the dendrite to convey the signal.
When Klyachko monitored electrical surges along axons in the fragile X mice, though, he discovered that they lasted significantly longer. This caused release of more of neurotransmitters from the axon. When it should have stopped talking, the axon continued to chatter.
“The axons are putting out much more neurotransmitter than they should, and we think this confuses the system and overloads the circuitry,” Klyachko explains. “It may also create problems in terms of brain cells using up their resources much more quickly than they normally would.”
Infusing synthetic copies of the gene’s protein, called FMRP, into brain cells from the mouse model rapidly restored the electrical surges to their normal length.
Additional experiments revealed that FMRP works by interacting with one of the biggest channels on the surfaces of axons. These channels let electrically charged potassium ions into the axons, helping to shape and control the duration of the electrical surge.
In healthy brain cells, the main function of these channels is to prevent the electrical surge from getting too long. With FMRP gone, the channel is active for a shorter time, prolonging the surge and overwhelming the dendrite with too much chatter.
Klyachko and his colleagues are now studying the connections between FMRP and the channel it interacts with in axons. They hope to learn more about how information is encoded and processed at the level of individual brain cells. These insights one day may help clinicians better diagnose and treat many kinds of mental disorders.
Human cognition depends upon slow-firing neurons
Good mental health and clear thinking depend upon our ability to store and manipulate thoughts on a sort of “mental sketch pad.” In a new study, Yale School of Medicine researchers describe the molecular basis of this ability — the hallmark of human cognition — and describe how a breakdown of the system contributes to diseases such as schizophrenia and Alzheimer’s disease.
“Insults to these highly evolved cortical circuits impair the ability to create and maintain our mental representations of the world, which is the basis of higher cognition,” said Amy Arnsten, professor of neurobiology and senior author of the paper published in the Feb. 20 issue of the journal Neuron.
High-order thinking depends upon our ability to generate mental representations in our brains without any sensory stimulation from the environment. These cognitive abilities arise from highly evolved circuits in the prefrontal cortex. Mathematical models by former Yale neurobiologist Xiao-Jing Wang, now of New York University, predicted that in order to maintain these visual representations the prefrontal cortex must rely on a family of receptors that allow for slow, steady firing of neurons. The Yale scientists show that NMDA-NR2B receptors involved in glutamate signaling regulate this neuronal firing. These receptors, studied at Yale for more than a decade, are responsible for activity of highly evolved brain circuits found especially in primates.
Earlier studies have shown these types of NMDA receptors are often altered in patients with schizophrenia. The Neuron study suggests that those suffering from the disease may be unable to hold onto a stable view of the world. Also, these receptors seem to be altered in Alzheimer’s patients, which may contribute to the cognitive deficits of dementia.
The lab of Dr. John Krystal, chair of the department of psychiatry at Yale, has found that the anesthetic ketamine, abused as a street drug, blocks NMDA receptors and can mimic some of the symptoms of schizophrenia. The current study in Neuron shows that ketamine may reduce the firing of the same higher-order neural circuits that are decimated in schizophrenia.
“Identifying the receptor needed for higher cognition may help us to understand why certain genetic insults lead to cognitive impairment and will help us to develop strategies for treating these debilitating disorders,” Arnsten said.