Neuroscience

Articles and news from the latest research reports.

Posts tagged science

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BrainBow is a technique where cells are made to express several fluorescent proteins, in essentially random amounts. The randomness derives from feedback loops in gene expression. Mixing of fluorescence wavelengths yields a remarkable colour contrast on the single-neuron level.

The method was originally developed by Jeff W. Lichtman and Joshua R. Sanes at the Department of Neurobiology, Harvard Medical School.

Read more about BrainBow on Wikipedia or an introduction at the Harvard Gazette.

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Filed under brain brainbow neuron hippocampus cerebellum cortex brain stem neuroscience science

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Poor sleep in old age prevents the brain from storing memories
The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But for the first time, scientists at the University of California, Berkeley, have found a link between these hallmark maladies of old age. Their discovery opens the door to boosting the quality of sleep in elderly people to improve memory.
UC Berkeley neuroscientists have found that the slow brain waves generated during the deep, restorative sleep we typically experience in youth play a key role in transporting memories from the hippocampus – which provides short-term storage for memories – to the prefrontal cortex’s longer term “hard drive.”
However, in older adults, memories may be getting stuck in the hippocampus due to the poor quality of deep ‘slow wave’ sleep, and are then overwritten by new memories, the findings suggest.
“What we have discovered is a dysfunctional pathway that helps explain the relationship between brain deterioration, sleep disruption and memory loss as we get older – and with that, a potentially new treatment avenue,” said UC Berkeley sleep researcher Matthew Walker, an associate professor of psychology and neuroscience at UC Berkeley and senior author of the study published in the journal Nature Neuroscience.

Poor sleep in old age prevents the brain from storing memories

The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But for the first time, scientists at the University of California, Berkeley, have found a link between these hallmark maladies of old age. Their discovery opens the door to boosting the quality of sleep in elderly people to improve memory.

UC Berkeley neuroscientists have found that the slow brain waves generated during the deep, restorative sleep we typically experience in youth play a key role in transporting memories from the hippocampus – which provides short-term storage for memories – to the prefrontal cortex’s longer term “hard drive.”

However, in older adults, memories may be getting stuck in the hippocampus due to the poor quality of deep ‘slow wave’ sleep, and are then overwritten by new memories, the findings suggest.

“What we have discovered is a dysfunctional pathway that helps explain the relationship between brain deterioration, sleep disruption and memory loss as we get older – and with that, a potentially new treatment avenue,” said UC Berkeley sleep researcher Matthew Walker, an associate professor of psychology and neuroscience at UC Berkeley and senior author of the study published in the journal Nature Neuroscience.

Filed under brainwaves sleep memory prefrontal cortex frontal lobe aging neuroscience science

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Study Sheds Light on the Complexity of Gene Therapy for Congenital Blindness
Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered. Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.
LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.
“We all hoped that the gene injections cured both components – re-establishing the cycle of vision and also preventing further loss of cells to the second disease component” said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.
Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. “In other words, gene therapy improved vision but did not slow or halt the progression of cell loss,” commented Cideciyan.
“These unexpected observations should help to advance the current treatment by making it better and longer lasting,” commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. “Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA.”
(Image: bigstockphoto)

Study Sheds Light on the Complexity of Gene Therapy for Congenital Blindness

Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered. Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

“We all hoped that the gene injections cured both components – re-establishing the cycle of vision and also preventing further loss of cells to the second disease component” said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. “In other words, gene therapy improved vision but did not slow or halt the progression of cell loss,” commented Cideciyan.

“These unexpected observations should help to advance the current treatment by making it better and longer lasting,” commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. “Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA.”

(Image: bigstockphoto)

Filed under photoreceptors retina retinal degeneration congenital blindness gene therapy science

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Evidence Mounts for Role of Mutated Genes in Development of Schizophrenia
Johns Hopkins researchers have identified a rare gene mutation in a single family with a high rate of schizophrenia, adding to evidence that abnormal genes play a role in the development of the disease.
The researchers, in a report published in the journal Molecular Psychiatry, say that family members with the mutation in the gene Neuronal PAS domain protein 3 (NPAS3) appear at high risk of developing schizophrenia or another debilitating mental illnesses.
Normally functioning NPAS3 regulates the development of healthy neurons, especially in a region of the brain known as the hippocampus, which appears to be affected in schizophrenia. The Johns Hopkins researchers say they have evidence that the mutation found in the family may lead to abnormal activity of NPAS3, which has implications for brain development and function.
"Understanding the molecular and biological pathways of schizophrenia is a powerful way to advance the development of treatments that have fewer side effects and work better than the treatments now available," says study leader Frederick C. Nucifora Jr., Ph.D., D.O., M.H.S., an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We could definitely use better medicines."

Evidence Mounts for Role of Mutated Genes in Development of Schizophrenia

Johns Hopkins researchers have identified a rare gene mutation in a single family with a high rate of schizophrenia, adding to evidence that abnormal genes play a role in the development of the disease.

The researchers, in a report published in the journal Molecular Psychiatry, say that family members with the mutation in the gene Neuronal PAS domain protein 3 (NPAS3) appear at high risk of developing schizophrenia or another debilitating mental illnesses.

Normally functioning NPAS3 regulates the development of healthy neurons, especially in a region of the brain known as the hippocampus, which appears to be affected in schizophrenia. The Johns Hopkins researchers say they have evidence that the mutation found in the family may lead to abnormal activity of NPAS3, which has implications for brain development and function.

"Understanding the molecular and biological pathways of schizophrenia is a powerful way to advance the development of treatments that have fewer side effects and work better than the treatments now available," says study leader Frederick C. Nucifora Jr., Ph.D., D.O., M.H.S., an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We could definitely use better medicines."

Filed under schizophrenia mental illness mental health mutation genetics neuroscience science

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Cell biologists show molecular forces are key to proper cell division
Studies led by assistant professor of Biology Thomas Maresca are revealing new details about a molecular surveillance system that helps detect and correct errors in cell division that can lead to cell death or human diseases. Findings are reported in the current issue of the Journal of Cell Biology.
The purpose of cell division is to evenly distribute the genome between two daughter cells. To achieve this, every chromosome must properly interact with a football-shaped structure called the spindle. However, interaction errors between the chromosomes and spindle during division are amazingly common, occurring in 86 to 90 percent of chromosomes, says Maresca, an expert in mitosis.
“This is not quite so surprising when you realize that every single one of the 46 chromosomes has to get into perfect position every time a cell divides,” he notes. The key to flawless cell division is to correct dangerous interactions before the cell splits in two.
Working with fruit fly tissue culture cells, Maresca and graduate students Stuart Cane and Anna Ye have developed a way to watch and record images of the key players in cell division including microtubule filaments that form the mitotic spindle and sites called kinetochores that mediate chromosome-microtubule interactions. They also examined the contribution of a force generated by molecular engines called the polar ejection force (PEF), which is thought to help line up the chromosomes in the middle of the spindle for division. For the first time, they directly tested and quantified how PEF, in particular, influences tension at kinetochores and affects error correction in mitosis.
“We also now have a powerful new assay to get at how this tension regulates kinetochore-microtubule interactions,” Maresca adds. “We knew forces and tension regulated this process, but we didn’t understand exactly how. With the new technique, we can start to dissect out how tension modulates error correction to repair the many erroneous attachment intermediates that form during division.”

Cell biologists show molecular forces are key to proper cell division

Studies led by assistant professor of Biology Thomas Maresca are revealing new details about a molecular surveillance system that helps detect and correct errors in cell division that can lead to cell death or human diseases. Findings are reported in the current issue of the Journal of Cell Biology.

The purpose of cell division is to evenly distribute the genome between two daughter cells. To achieve this, every chromosome must properly interact with a football-shaped structure called the spindle. However, interaction errors between the chromosomes and spindle during division are amazingly common, occurring in 86 to 90 percent of chromosomes, says Maresca, an expert in mitosis.

“This is not quite so surprising when you realize that every single one of the 46 chromosomes has to get into perfect position every time a cell divides,” he notes. The key to flawless cell division is to correct dangerous interactions before the cell splits in two.

Working with fruit fly tissue culture cells, Maresca and graduate students Stuart Cane and Anna Ye have developed a way to watch and record images of the key players in cell division including microtubule filaments that form the mitotic spindle and sites called kinetochores that mediate chromosome-microtubule interactions. They also examined the contribution of a force generated by molecular engines called the polar ejection force (PEF), which is thought to help line up the chromosomes in the middle of the spindle for division. For the first time, they directly tested and quantified how PEF, in particular, influences tension at kinetochores and affects error correction in mitosis.

“We also now have a powerful new assay to get at how this tension regulates kinetochore-microtubule interactions,” Maresca adds. “We knew forces and tension regulated this process, but we didn’t understand exactly how. With the new technique, we can start to dissect out how tension modulates error correction to repair the many erroneous attachment intermediates that form during division.”

Filed under cell division chromosomes fruit fly kinetochores trisomy mitosis cells science

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Stroke Survivors with PTSD More Likely to Avoid Treatment
A new survey of stroke survivors has shown that those with post-traumatic stress disorder (PTSD) are less likely to adhere to treatment regimens that reduce the risk of an additional stroke. Researchers found that 65 percent of stroke survivors with PTSD failed to adhere to treatment, compared with 33 percent of those without PTSD. The survey also suggests that nonadherence in PTSD patients is partly explained by increased ambivalence toward medication. Among stroke survivors with PTSD, approximately one in three (38 percent) had concerns about their medications. Results of the study, led by Columbia University Medical Center researchers, are published today in the British Journal of Health Psychology.
According to data from the American Stroke Association, nearly 795,000 Americans each year suffer a new or recurrent stroke. Stroke is the fourth-leading cause of death and the top cause of disability in the United States. Survivors of strokes are often prescribed treatment regiments, including antiplatelet agents, antihypertensive agents, and statins, which help reduce the risk of subsequent strokes. Previous research has shown that PTSD triggered by medical events—which affects 18 percent of stroke survivors—may impair recovery.
“Unfortunately, too many stroke survivors are not compliant with these regimens, even though we know that adherence to post-stroke treatment regimens is one of the most important components of reducing the risk of a future stroke,” said Ian M. Kronish, MD, MPH, assistant professor of medicine (Center for Behavioral Cardiovascular Health) and one of the study’s authors.
“For those with PTSD, this study shows that concerns about medications are a significant barrier to treatment adherence. Stroke survivors should be assessed for concerns about medications and PTSD symptoms, so that interventions may be introduced as early as possible to get patients back on track to avoid future stroke events.”

Stroke Survivors with PTSD More Likely to Avoid Treatment

A new survey of stroke survivors has shown that those with post-traumatic stress disorder (PTSD) are less likely to adhere to treatment regimens that reduce the risk of an additional stroke. Researchers found that 65 percent of stroke survivors with PTSD failed to adhere to treatment, compared with 33 percent of those without PTSD. The survey also suggests that nonadherence in PTSD patients is partly explained by increased ambivalence toward medication. Among stroke survivors with PTSD, approximately one in three (38 percent) had concerns about their medications. Results of the study, led by Columbia University Medical Center researchers, are published today in the British Journal of Health Psychology.

According to data from the American Stroke Association, nearly 795,000 Americans each year suffer a new or recurrent stroke. Stroke is the fourth-leading cause of death and the top cause of disability in the United States. Survivors of strokes are often prescribed treatment regiments, including antiplatelet agents, antihypertensive agents, and statins, which help reduce the risk of subsequent strokes. Previous research has shown that PTSD triggered by medical events—which affects 18 percent of stroke survivors—may impair recovery.

“Unfortunately, too many stroke survivors are not compliant with these regimens, even though we know that adherence to post-stroke treatment regimens is one of the most important components of reducing the risk of a future stroke,” said Ian M. Kronish, MD, MPH, assistant professor of medicine (Center for Behavioral Cardiovascular Health) and one of the study’s authors.

“For those with PTSD, this study shows that concerns about medications are a significant barrier to treatment adherence. Stroke survivors should be assessed for concerns about medications and PTSD symptoms, so that interventions may be introduced as early as possible to get patients back on track to avoid future stroke events.”

Filed under PTSD stress stroke treatment medications psychology neuroscience science

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Repeated aggressions trigger social aversion in mice
One of the mechanisms involved in the onset of stress-induced depression has been highlighted in mice by researchers from CNRS, Inserm and UPMC. They have determined the role of the corticosterone (stress hormone) receptor, in the long-term behavioral change triggered by chronic stress. In mice subject to repeated aggressions, this receptor participates in the development of social aversion by controlling the release of dopamine, a key chemical messenger. If this receptor is blocked, the animals become “resilient”: although anxious, they overcome the trauma and no longer avoid contact with their fellow creatures. This work is published in Science on 18 January 2013.

Repeated aggressions trigger social aversion in mice

One of the mechanisms involved in the onset of stress-induced depression has been highlighted in mice by researchers from CNRS, Inserm and UPMC. They have determined the role of the corticosterone (stress hormone) receptor, in the long-term behavioral change triggered by chronic stress. In mice subject to repeated aggressions, this receptor participates in the development of social aversion by controlling the release of dopamine, a key chemical messenger. If this receptor is blocked, the animals become “resilient”: although anxious, they overcome the trauma and no longer avoid contact with their fellow creatures. This work is published in Science on 18 January 2013.

Filed under social aversion corticosterone stress aggression neurotransmitters dopamine neuroscience science

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Scientists discover how epigenetic information could be inherited
New research reveals a potential way for how parents’ experiences could be passed to their offspring’s genes. The research was published in the journal Science.
Epigenetics is a system that turns our genes on and off. The process works by chemical tags, known as epigenetic marks, attaching to DNA and telling a cell to either use or ignore a particular gene.
The most common epigenetic mark is a methyl group. When these groups fasten to DNA through a process called methylation they block the attachment of proteins which normally turn the genes on. As a result, the gene is turned off.
Scientists have witnessed epigenetic inheritance, the observation that offspring may inherit altered traits due to their parents’ past experiences. For example, historical incidences of famine have resulted in health effects on the children and grandchildren of individuals who had restricted diets, possibly because of inheritance of altered epigenetic marks caused by a restricted diet.
However, it is thought that between each generation the epigenetic marks are erased in cells called primordial gene cells (PGC), the precursors to sperm and eggs. This ‘reprogramming’ allows all genes to be read afresh for each new person – leaving scientists to question how epigenetic inheritance could occur.
The new Cambridge study initially discovered how the DNA methylation marks are erased in PGCs, a question that has been under intense investigation over the past 10 years. The methylation marks are converted to hydroxymethylation which is then progressively diluted out as the cells divide. This process turns out to be remarkably efficient and seems to reset the genes for each new generation. Understanding the mechanism of epigenetic resetting could be exploited to deal with adult diseases linked with an accumulation of aberrant epigenetic marks, such as cancers, or in ‘rejuvenating’ aged cells.
However, the researchers, who were funded by the Wellcome Trust, also found that some rare methylation can ‘escape’ the reprogramming process and can thus be passed on to offspring – revealing how epigenetic inheritance could occur. This is important because aberrant methylation could accumulate at genes during a lifetime in response to environmental factors, such as chemical exposure or nutrition, and can cause abnormal use of genes, leading to disease. If these marks are then inherited by offspring, their genes could also be affected.

Scientists discover how epigenetic information could be inherited

New research reveals a potential way for how parents’ experiences could be passed to their offspring’s genes. The research was published in the journal Science.

Epigenetics is a system that turns our genes on and off. The process works by chemical tags, known as epigenetic marks, attaching to DNA and telling a cell to either use or ignore a particular gene.

The most common epigenetic mark is a methyl group. When these groups fasten to DNA through a process called methylation they block the attachment of proteins which normally turn the genes on. As a result, the gene is turned off.

Scientists have witnessed epigenetic inheritance, the observation that offspring may inherit altered traits due to their parents’ past experiences. For example, historical incidences of famine have resulted in health effects on the children and grandchildren of individuals who had restricted diets, possibly because of inheritance of altered epigenetic marks caused by a restricted diet.

However, it is thought that between each generation the epigenetic marks are erased in cells called primordial gene cells (PGC), the precursors to sperm and eggs. This ‘reprogramming’ allows all genes to be read afresh for each new person – leaving scientists to question how epigenetic inheritance could occur.

The new Cambridge study initially discovered how the DNA methylation marks are erased in PGCs, a question that has been under intense investigation over the past 10 years. The methylation marks are converted to hydroxymethylation which is then progressively diluted out as the cells divide. This process turns out to be remarkably efficient and seems to reset the genes for each new generation. Understanding the mechanism of epigenetic resetting could be exploited to deal with adult diseases linked with an accumulation of aberrant epigenetic marks, such as cancers, or in ‘rejuvenating’ aged cells.

However, the researchers, who were funded by the Wellcome Trust, also found that some rare methylation can ‘escape’ the reprogramming process and can thus be passed on to offspring – revealing how epigenetic inheritance could occur. This is important because aberrant methylation could accumulate at genes during a lifetime in response to environmental factors, such as chemical exposure or nutrition, and can cause abnormal use of genes, leading to disease. If these marks are then inherited by offspring, their genes could also be affected.

Filed under epigenetics genes inheritance DNA primordial gene cells DNA methylation science

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Frontiers publishes systematic review on the effects of yoga on major psychiatric disorders
Yoga has positive effects on mild depression and sleep complaints, even in the absence of drug treatments, and improves symptoms associated with schizophrenia and ADHD in patients on medication, according to a systematic review of the exercise on major clinical psychiatric disorders.
Published in the open-access journal, Frontiers in Psychiatry, on January 25th, 2013, the review of more than one hundred studies focusing on 16 high-quality controlled studies looked at the effects of yoga on depression, schizophrenia, ADHD, sleep complaints, eating disorders and cognition problems.
(Image: Corbis)

Frontiers publishes systematic review on the effects of yoga on major psychiatric disorders

Yoga has positive effects on mild depression and sleep complaints, even in the absence of drug treatments, and improves symptoms associated with schizophrenia and ADHD in patients on medication, according to a systematic review of the exercise on major clinical psychiatric disorders.

Published in the open-access journal, Frontiers in Psychiatry, on January 25th, 2013, the review of more than one hundred studies focusing on 16 high-quality controlled studies looked at the effects of yoga on depression, schizophrenia, ADHD, sleep complaints, eating disorders and cognition problems.

(Image: Corbis)

Filed under meditation yoga psychiatric disorders mental illness depression science

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