Post has attachment
Bacteria found in Alzheimer’s brains
Researchers in the UK have used DNA sequencing to examine bacteria in post-mortem brains from patients with Alzheimer’s disease. Their findings suggest increased bacterial populations and different proportions of specific bacteria in Alzheimer’s, compared with healthy brains. The findings may support evidence that bacterial infection and inflammation in the brain could contribute to Alzheimer’s disease.
Alzheimer’s disease is a neurodegenerative disease that results in cognitive decline, and eventually death. In the brain, the disease causes neurons to die and break down, and involves high levels of a peptide called amyloid and aggregations of a protein called tau. However, scientists are coming to appreciate that inflammation may also play a role.
“Alzheimer’s brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate,” says David Emery, a researcher from the University of Bristol, and an author on the study, which was published in Frontiers in Aging Neuroscience.
Journal article:
https://www.frontiersin.org/articles/10.3389/fnagi.2017.00195/full
Source:
https://blog.frontiersin.org/2017/07/24/frontiers-in-aging-neuroscience-bacteria-found-in-alzheimers-brains/
#neuroscience #alzheimers #research #bacteria #health #medicine
Researchers in the UK have used DNA sequencing to examine bacteria in post-mortem brains from patients with Alzheimer’s disease. Their findings suggest increased bacterial populations and different proportions of specific bacteria in Alzheimer’s, compared with healthy brains. The findings may support evidence that bacterial infection and inflammation in the brain could contribute to Alzheimer’s disease.
Alzheimer’s disease is a neurodegenerative disease that results in cognitive decline, and eventually death. In the brain, the disease causes neurons to die and break down, and involves high levels of a peptide called amyloid and aggregations of a protein called tau. However, scientists are coming to appreciate that inflammation may also play a role.
“Alzheimer’s brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate,” says David Emery, a researcher from the University of Bristol, and an author on the study, which was published in Frontiers in Aging Neuroscience.
Journal article:
https://www.frontiersin.org/articles/10.3389/fnagi.2017.00195/full
Source:
https://blog.frontiersin.org/2017/07/24/frontiers-in-aging-neuroscience-bacteria-found-in-alzheimers-brains/
#neuroscience #alzheimers #research #bacteria #health #medicine
Post has attachment
How neurons sense our everyday life
Researchers from King’s College London have discovered a molecular mechanism that enables neuronal connections to change through experience, thus fueling learning and memory formation. The findings are published in the journal Neuron and have the potential to reveal new therapeutic strategies for neurological and psychiatric disorders.
One of the most remarkable features of our brain is its ability to sense and interpret the complex environment of everyday life. To accomplish this, brain circuits undergo a process that involves experience-dependent plasticity, a fundamental mechanism through which the nervous system adapts to sensory experience and which is at the root of our capacity to learn as well as encode and retain memories. As an example, all babies are born with the capacity to develop language but their ability to communicate verbally will depend on their exposure to language during the early stages of development.
Impairment of experience-dependent plasticity has been shown to be a feature of many neurological and psychiatric disorders including depression, bipolar disorder and schizophrenia. As such, unravelling key molecular players in this form of plasticity may pave the way for new treatments.
Previous studies have shown that a special group of neurons present in the cerebral cortex called PV+ interneurons (a population of neurons that communicate with each other through deactivating chemical and electrical signals and express a protein called parvalbumin), are able to change in response to stimulus from the environment. However, until now the cellular and molecular mechanisms regulating this adaptability were largely unknown.
In their new study, the multidisciplinary team of researchers led by the Centre for Developmental Neurobiology (CDN) and MRC Centre for Neurodevelopmental Disorders (MRC CNDD) at the Institute of Psychiatry, Psychology & Neuroscience, found that this adaptability is shaped by a specific protein called Brevican. Moreover, loss of this protein leads to deficits in short-term spatial memory, the part of memory responsible for remembering different locations as well as spatial relations between objects.
Source:
https://www.kcl.ac.uk/ioppn/news/records/2017/07-July/How-neurons-sense-our-everyday-life.aspx
Journal article:
http://www.cell.com/neuron/fulltext/S0896-6273(17)30552-4
#interneurons #plasticity #parvalbumin #brevican #neuroscience #science
Researchers from King’s College London have discovered a molecular mechanism that enables neuronal connections to change through experience, thus fueling learning and memory formation. The findings are published in the journal Neuron and have the potential to reveal new therapeutic strategies for neurological and psychiatric disorders.
One of the most remarkable features of our brain is its ability to sense and interpret the complex environment of everyday life. To accomplish this, brain circuits undergo a process that involves experience-dependent plasticity, a fundamental mechanism through which the nervous system adapts to sensory experience and which is at the root of our capacity to learn as well as encode and retain memories. As an example, all babies are born with the capacity to develop language but their ability to communicate verbally will depend on their exposure to language during the early stages of development.
Impairment of experience-dependent plasticity has been shown to be a feature of many neurological and psychiatric disorders including depression, bipolar disorder and schizophrenia. As such, unravelling key molecular players in this form of plasticity may pave the way for new treatments.
Previous studies have shown that a special group of neurons present in the cerebral cortex called PV+ interneurons (a population of neurons that communicate with each other through deactivating chemical and electrical signals and express a protein called parvalbumin), are able to change in response to stimulus from the environment. However, until now the cellular and molecular mechanisms regulating this adaptability were largely unknown.
In their new study, the multidisciplinary team of researchers led by the Centre for Developmental Neurobiology (CDN) and MRC Centre for Neurodevelopmental Disorders (MRC CNDD) at the Institute of Psychiatry, Psychology & Neuroscience, found that this adaptability is shaped by a specific protein called Brevican. Moreover, loss of this protein leads to deficits in short-term spatial memory, the part of memory responsible for remembering different locations as well as spatial relations between objects.
Source:
https://www.kcl.ac.uk/ioppn/news/records/2017/07-July/How-neurons-sense-our-everyday-life.aspx
Journal article:
http://www.cell.com/neuron/fulltext/S0896-6273(17)30552-4
#interneurons #plasticity #parvalbumin #brevican #neuroscience #science
Post has attachment
Brain Responds Differently to Food Rewards in Bulimia Nervosa
Findings could contribute to new treatment therapies targeting specific brain pathways
Researchers at University of California San Diego School of Medicine have discovered differences in how the brain responds to food rewards in individuals with a history of bulimia nervosa (BN), an eating disorder characterized by frequent episodes of binge eating followed by efforts of purging to avoid weight gain. The findings further define specific brain mechanisms involved in eating disorders and could help lead to new treatment therapies.
Metabolic (hunger) and hedonic (reward) brain mechanisms both contribute to the regulation of eating. The findings, published July 10 in the Journal of Abnormal Psychology, address the question of whether binge eating in BN results from disruption of one or both mechanisms, or is the product of their interaction.
“Our study suggests that adults with bulimia nervosa may have elevated reward-related brain activation in response to taste. This altered neural response may explain why these individuals tend to remain driven to eat even when not hungry,” said Alice V. Ely, PhD, principal author of the study in the Department of Psychiatry at UC San Diego School of Medicine.
Source & further reading:
https://health.ucsd.edu/news/releases/Pages/2017-07-10-brain-responds-differently-to-food-rewards-in-bulimia-nervosa.aspx
#neuroscience #eatingdisorders #bulimianervosa #research
Findings could contribute to new treatment therapies targeting specific brain pathways
Researchers at University of California San Diego School of Medicine have discovered differences in how the brain responds to food rewards in individuals with a history of bulimia nervosa (BN), an eating disorder characterized by frequent episodes of binge eating followed by efforts of purging to avoid weight gain. The findings further define specific brain mechanisms involved in eating disorders and could help lead to new treatment therapies.
Metabolic (hunger) and hedonic (reward) brain mechanisms both contribute to the regulation of eating. The findings, published July 10 in the Journal of Abnormal Psychology, address the question of whether binge eating in BN results from disruption of one or both mechanisms, or is the product of their interaction.
“Our study suggests that adults with bulimia nervosa may have elevated reward-related brain activation in response to taste. This altered neural response may explain why these individuals tend to remain driven to eat even when not hungry,” said Alice V. Ely, PhD, principal author of the study in the Department of Psychiatry at UC San Diego School of Medicine.
Source & further reading:
https://health.ucsd.edu/news/releases/Pages/2017-07-10-brain-responds-differently-to-food-rewards-in-bulimia-nervosa.aspx
#neuroscience #eatingdisorders #bulimianervosa #research
Post has attachment
Menstruation doesn't change how your brain works -- period
A study published in Frontiers in Behavioral Neuroscience is setting out to change the way we think about the menstrual cycle. While it’s often been assumed that anyone who’s menstruating isn’t working at top mental pitch, Professor Brigitte Leeners and her team of researchers have found evidence to suggest that that’s not the case.
They examined three aspects of cognition across two menstrual cycles, and found that the levels of oestrogen, progesterone and testosterone in your system have no impact on your working memory, cognitive bias or ability to pay attention to two things at once. While some hormones were associated with changes across one cycle in some of the women taking part, these effects didn’t repeat in the following cycle. Overall, none of the hormones the team studied had any replicable, consistent effect on study participants’ cognition.
Professor Leeners, team lead, said: “As a specialist in reproductive medicine and a psychotherapist, I deal with many women who have the impression that the menstrual cycle influences their well-being and cognitive performance.” Wondering if this anecdotal evidence could be scientifically proven - and questioning the methodology of many existing studies on the subject - the team set out to shed some light on this controversial topic.
The study uses a much larger sample than usual, and (unlike most similar studies) follows women across two consecutive menstrual cycles. The team, working from the Medical School Hannover and University Hospital Zürich, recruited 68 women to undergo detailed monitoring to investigate changes in three selected cognitive processes at different stages in the menstrual cycle. While analysis of the results from the first cycle suggested that cognitive bias and attention were affected, these results weren’t replicated in the second cycle. The team looked for differences in performance between individuals and changes in individuals’ performance over time, and found none.
Professor Leeners said, “The hormonal changes related to the menstrual cycle do not show any association with cognitive performance. Although there might be individual exceptions, women’s cognitive performance is in general not disturbed by hormonal changes occurring with the menstrual cycle.”
Professor Leeners cautions, however, that there’s more work to do. While this study represents a meaningful step forward, larger samples, bigger subsamples of women with hormone disorders, and further cognitive tests would provide a fuller picture of the way that the menstrual cycle affects the brain. In the meantime, Professor Leeners hopes her team’s work will start the long process of changing minds about menstruation.
Source:
https://www.eurekalert.org/pub_releases/2017-07/f-mdc062717.php
Paper:
https://www.frontiersin.org/articles/10.3389/fnbeh.2017.00120/full
#menstrualcycle #cognitivefunction #workingmemory #neuroscience #science
A study published in Frontiers in Behavioral Neuroscience is setting out to change the way we think about the menstrual cycle. While it’s often been assumed that anyone who’s menstruating isn’t working at top mental pitch, Professor Brigitte Leeners and her team of researchers have found evidence to suggest that that’s not the case.
They examined three aspects of cognition across two menstrual cycles, and found that the levels of oestrogen, progesterone and testosterone in your system have no impact on your working memory, cognitive bias or ability to pay attention to two things at once. While some hormones were associated with changes across one cycle in some of the women taking part, these effects didn’t repeat in the following cycle. Overall, none of the hormones the team studied had any replicable, consistent effect on study participants’ cognition.
Professor Leeners, team lead, said: “As a specialist in reproductive medicine and a psychotherapist, I deal with many women who have the impression that the menstrual cycle influences their well-being and cognitive performance.” Wondering if this anecdotal evidence could be scientifically proven - and questioning the methodology of many existing studies on the subject - the team set out to shed some light on this controversial topic.
The study uses a much larger sample than usual, and (unlike most similar studies) follows women across two consecutive menstrual cycles. The team, working from the Medical School Hannover and University Hospital Zürich, recruited 68 women to undergo detailed monitoring to investigate changes in three selected cognitive processes at different stages in the menstrual cycle. While analysis of the results from the first cycle suggested that cognitive bias and attention were affected, these results weren’t replicated in the second cycle. The team looked for differences in performance between individuals and changes in individuals’ performance over time, and found none.
Professor Leeners said, “The hormonal changes related to the menstrual cycle do not show any association with cognitive performance. Although there might be individual exceptions, women’s cognitive performance is in general not disturbed by hormonal changes occurring with the menstrual cycle.”
Professor Leeners cautions, however, that there’s more work to do. While this study represents a meaningful step forward, larger samples, bigger subsamples of women with hormone disorders, and further cognitive tests would provide a fuller picture of the way that the menstrual cycle affects the brain. In the meantime, Professor Leeners hopes her team’s work will start the long process of changing minds about menstruation.
Source:
https://www.eurekalert.org/pub_releases/2017-07/f-mdc062717.php
Paper:
https://www.frontiersin.org/articles/10.3389/fnbeh.2017.00120/full
#menstrualcycle #cognitivefunction #workingmemory #neuroscience #science
Post has attachment
The brain’s fight and flight responses to social threat
A study published in eNeuro exploring the neural correlates of the ‘fight-or-flight’ response finds that people who choose to flee perceive a greater threat, which leads them to mentally and behaviorally disengage from the situation.
Macià Buades-Rotger and colleagues designed a Lord of the Rings-themed experiment in which 36 female participants competed as Frodo against two confederates playing as Sauron and Saruman in a reaction time task.
Participants could choose to avoid a limited number of encounters with their opponents by “putting the Ring on.” If they chose to stay and fight, they had to select the intensity of a sound blast (retaliation) that would be directed toward their opponent if the participant won the task by having a quicker reaction time. The task was set so that participants lost two-thirds of trials, and each opponent gave either high or low sound blasts.
The authors found that brain regions associated with thinking about the mental state of others were engaged when deciding to flee. However, when facing the highly provoking opponent, the “flight” response was associated with reduced activity in these regions and increased activity in the amygdala, indicating increased threat detection.
Journal article:
http://www.eneuro.org/content/4/3/ENEURO.0337-16.2017
Source & further reading:
https://www.eurekalert.org/pub_releases/2017-06/sfn-tbf062117.php
Image: When avoiding the highly provoking opponent there was increased activity in the amygdala and reduced activation in brain regions typically recruited when thinking about others’ feelings and intentions. This pattern suggests that avoidance is associated with enhanced threat detection and reduced perspective-taking.
Credit: Macià Buades-Rotger
#amygdala #neuroimaging #orbitofrontalcortex #prefrontalcortex #socialbehavior #neuroscience
A study published in eNeuro exploring the neural correlates of the ‘fight-or-flight’ response finds that people who choose to flee perceive a greater threat, which leads them to mentally and behaviorally disengage from the situation.
Macià Buades-Rotger and colleagues designed a Lord of the Rings-themed experiment in which 36 female participants competed as Frodo against two confederates playing as Sauron and Saruman in a reaction time task.
Participants could choose to avoid a limited number of encounters with their opponents by “putting the Ring on.” If they chose to stay and fight, they had to select the intensity of a sound blast (retaliation) that would be directed toward their opponent if the participant won the task by having a quicker reaction time. The task was set so that participants lost two-thirds of trials, and each opponent gave either high or low sound blasts.
The authors found that brain regions associated with thinking about the mental state of others were engaged when deciding to flee. However, when facing the highly provoking opponent, the “flight” response was associated with reduced activity in these regions and increased activity in the amygdala, indicating increased threat detection.
Journal article:
http://www.eneuro.org/content/4/3/ENEURO.0337-16.2017
Source & further reading:
https://www.eurekalert.org/pub_releases/2017-06/sfn-tbf062117.php
Image: When avoiding the highly provoking opponent there was increased activity in the amygdala and reduced activation in brain regions typically recruited when thinking about others’ feelings and intentions. This pattern suggests that avoidance is associated with enhanced threat detection and reduced perspective-taking.
Credit: Macià Buades-Rotger
#amygdala #neuroimaging #orbitofrontalcortex #prefrontalcortex #socialbehavior #neuroscience
Post has attachment
Parkinson’s Is Partly An Autoimmune Disease, Study Finds
Researchers have found the first direct evidence that autoimmunity — in which the immune system attacks the body’s own tissues — plays a role in Parkinson’s disease, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response.
The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published in Nature.
“The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology, and pharmacology) at CUMC. “But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson’s, can activate the T cells involved in autoimmune attacks.
“It remains to be seen whether the immune response to alpha-synuclein is an initial cause of Parkinson’s or if it contributes to neuronal death and worsening symptoms after the onset of the disease,” said study co-leader Alessandro Sette, Dr. Biol. Sci., professor in the Center for Infectious Disease at La Jolla Institute for Allergy and Immunology in La Jolla, Calif. “These findings, however, could provide a much-needed diagnostic test for Parkinson’s disease and could help us to identify individuals at risk or in the early stages of the disease.”
Source and further reading:
http://newsroom.cumc.columbia.edu/blog/2017/06/21/parkinsons-is-partly-an-autoimmune-disease-study-finds/
Journal article:
http://www.nature.com/articles/nature22815
#neuroscience #Parkinson's #alphasynuclein #immunesystem #dopaminergicneurons
Researchers have found the first direct evidence that autoimmunity — in which the immune system attacks the body’s own tissues — plays a role in Parkinson’s disease, the neurodegenerative movement disorder. The findings raise the possibility that the death of neurons in Parkinson’s could be prevented by therapies that dampen the immune response.
The study, led by scientists at Columbia University Medical Center (CUMC) and the La Jolla Institute for Allergy and Immunology, was published in Nature.
“The idea that a malfunctioning immune system contributes to Parkinson’s dates back almost 100 years,” said study co-leader David Sulzer, PhD, professor of neurobiology (in psychiatry, neurology, and pharmacology) at CUMC. “But until now, no one has been able to connect the dots. Our findings show that two fragments of alpha-synuclein, a protein that accumulates in the brain cells of people with Parkinson’s, can activate the T cells involved in autoimmune attacks.
“It remains to be seen whether the immune response to alpha-synuclein is an initial cause of Parkinson’s or if it contributes to neuronal death and worsening symptoms after the onset of the disease,” said study co-leader Alessandro Sette, Dr. Biol. Sci., professor in the Center for Infectious Disease at La Jolla Institute for Allergy and Immunology in La Jolla, Calif. “These findings, however, could provide a much-needed diagnostic test for Parkinson’s disease and could help us to identify individuals at risk or in the early stages of the disease.”
Source and further reading:
http://newsroom.cumc.columbia.edu/blog/2017/06/21/parkinsons-is-partly-an-autoimmune-disease-study-finds/
Journal article:
http://www.nature.com/articles/nature22815
#neuroscience #Parkinson's #alphasynuclein #immunesystem #dopaminergicneurons
Post has attachment
Egocentric hearing: Study clarifies how we can tell where a sound is coming from
A new UCL and University of Nottingham study has found that most neurons in the brain’s auditory cortex detect where a sound is coming from relative to the head, but some are tuned to a sound source’s actual position in the world.
The study, published in PLOS Biology, looked at whether head movements change the responses of neurons that track sound location.
“Our brains can represent sound location in either an egocentric manner – for example, when I can tell that a phone is ringing to my left – or in an allocentric manner – hearing that the phone is on the table. If I move my head, neurons with an egocentric focus will respond differently, as the phone’s position relative to my ears has changed, while the allocentric neurons will maintain their response,” said the study’s first author, Dr Stephen Town (UCL Ear Institute).
The researchers monitored ferrets while they moved around a small arena surrounded by speakers that emitted clicking sounds. Electrodes monitored the firing rates of neurons in the ferrets’ auditory cortex, while LEDs were used to track the animals’ movement.
Among the neurons under investigation that picked up sound location, the study showed that most displayed egocentric orientations by tracking where a sound source was relative to the animal’s head, but approximately 20% of the spatially tuned neurons instead tracked a sound source’s actual location in the world, independent of the ferret’s head movements.
The researchers also found that neurons were more sensitive to sound location when the ferret’s head was moving quickly.
“Most previous research into how we determine where a sound is coming from used participants with fixed head positions, which failed to differentiate between egocentric and allocentric tuning. Here we found that both types coexist in the auditory cortex,” said the study’s senior author, Dr Jennifer Bizley (UCL Ear Institute).
The researchers say their findings could be helpful in the design of technologies involving augmented or virtual reality.
“We often hear sounds presented though earphones as being inside our heads, but our findings suggest sound sources could be created to appear externally, in the world, if designers incorporate information about body and head movements,” Dr Town said.
Source & further reading:
http://www.ucl.ac.uk/news/news-articles/0617/150617-egocentric-hearing
Journal article:
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2001878
#neuroscience #hearing #auditorycortex #animalbehavior #neurons #soundlocalization #research
A new UCL and University of Nottingham study has found that most neurons in the brain’s auditory cortex detect where a sound is coming from relative to the head, but some are tuned to a sound source’s actual position in the world.
The study, published in PLOS Biology, looked at whether head movements change the responses of neurons that track sound location.
“Our brains can represent sound location in either an egocentric manner – for example, when I can tell that a phone is ringing to my left – or in an allocentric manner – hearing that the phone is on the table. If I move my head, neurons with an egocentric focus will respond differently, as the phone’s position relative to my ears has changed, while the allocentric neurons will maintain their response,” said the study’s first author, Dr Stephen Town (UCL Ear Institute).
The researchers monitored ferrets while they moved around a small arena surrounded by speakers that emitted clicking sounds. Electrodes monitored the firing rates of neurons in the ferrets’ auditory cortex, while LEDs were used to track the animals’ movement.
Among the neurons under investigation that picked up sound location, the study showed that most displayed egocentric orientations by tracking where a sound source was relative to the animal’s head, but approximately 20% of the spatially tuned neurons instead tracked a sound source’s actual location in the world, independent of the ferret’s head movements.
The researchers also found that neurons were more sensitive to sound location when the ferret’s head was moving quickly.
“Most previous research into how we determine where a sound is coming from used participants with fixed head positions, which failed to differentiate between egocentric and allocentric tuning. Here we found that both types coexist in the auditory cortex,” said the study’s senior author, Dr Jennifer Bizley (UCL Ear Institute).
The researchers say their findings could be helpful in the design of technologies involving augmented or virtual reality.
“We often hear sounds presented though earphones as being inside our heads, but our findings suggest sound sources could be created to appear externally, in the world, if designers incorporate information about body and head movements,” Dr Town said.
Source & further reading:
http://www.ucl.ac.uk/news/news-articles/0617/150617-egocentric-hearing
Journal article:
http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2001878
#neuroscience #hearing #auditorycortex #animalbehavior #neurons #soundlocalization #research
Post has attachment
Insomnia genes found
An international team of researchers has found, for the first time, seven risk genes for insomnia. With this finding the researchers have taken an important step towards the unraveling of the biological mechanisms that cause insomnia.
In addition, the finding proves that insomnia is not, as is often claimed, a purely psychological condition. Nature Genetics published the results of this research.
Insomnia is probably the most common health complaint. Even after treatment, poor sleep remains a persistent vulnerability for many people. By having determined the risk genes, professors Danielle Posthuma (VU and VUmc) and Eus Van Someren (Netherlands Institute for Neuroscience, VU and VUmc), the lead researchers of this international project, have come closer to unraveling the biological mechanisms that cause the predisposition for insomnia.
In a sample of 113,006 individuals, the researchers found 7 genes for insomnia. These genes play a role in the regulation of transcription, the process where DNA is read in order to make an RNA copy of it, and exocytosis, the release of molecules by cells in order to communicate with their environment. One of the identified genes, MEIS1, has previously been related to two other sleep disorders: Periodic Limb Movements of Sleep (PLMS) and Restless Legs Syndrome (RLS).
By collaborating with Konrad Oexle and colleagues from the Institute of Neurogenomics at the Helmholtz Zentrum, München, Germany, the researchers could conclude that the genetic variants in the gene seem to contribute to all three disorders. Strikingly, PLMS and RLS are characterized by restless movement and sensation, respectively, whereas insomnia is characterized mainly by a restless stream of consciousness.
Professor Van Someren, specialized in sleep and insomnia, believes that the findings are the start of a path towards an understanding of insomnia at the level of communication within and between neurons, and thus towards finding new ways of treatment.
Source & further reading:
https://www.vu.nl/en/news-agenda/news/2017/apr-jun/insomnia-genes-found.aspx
Journal article:
https://www.nature.com/articles/ng.3888
#neuroscience #insomnia #sleepdisorders #research
An international team of researchers has found, for the first time, seven risk genes for insomnia. With this finding the researchers have taken an important step towards the unraveling of the biological mechanisms that cause insomnia.
In addition, the finding proves that insomnia is not, as is often claimed, a purely psychological condition. Nature Genetics published the results of this research.
Insomnia is probably the most common health complaint. Even after treatment, poor sleep remains a persistent vulnerability for many people. By having determined the risk genes, professors Danielle Posthuma (VU and VUmc) and Eus Van Someren (Netherlands Institute for Neuroscience, VU and VUmc), the lead researchers of this international project, have come closer to unraveling the biological mechanisms that cause the predisposition for insomnia.
In a sample of 113,006 individuals, the researchers found 7 genes for insomnia. These genes play a role in the regulation of transcription, the process where DNA is read in order to make an RNA copy of it, and exocytosis, the release of molecules by cells in order to communicate with their environment. One of the identified genes, MEIS1, has previously been related to two other sleep disorders: Periodic Limb Movements of Sleep (PLMS) and Restless Legs Syndrome (RLS).
By collaborating with Konrad Oexle and colleagues from the Institute of Neurogenomics at the Helmholtz Zentrum, München, Germany, the researchers could conclude that the genetic variants in the gene seem to contribute to all three disorders. Strikingly, PLMS and RLS are characterized by restless movement and sensation, respectively, whereas insomnia is characterized mainly by a restless stream of consciousness.
Professor Van Someren, specialized in sleep and insomnia, believes that the findings are the start of a path towards an understanding of insomnia at the level of communication within and between neurons, and thus towards finding new ways of treatment.
Source & further reading:
https://www.vu.nl/en/news-agenda/news/2017/apr-jun/insomnia-genes-found.aspx
Journal article:
https://www.nature.com/articles/ng.3888
#neuroscience #insomnia #sleepdisorders #research
Post has attachment
Why does an anesthetic make us lose consciousness?
To date, researchers assumed that anesthetics interrupt signal transmission between different areas of the brain and that is why we lose consciousness. Neuroscientists at Goethe University Frankfurt and the Max Planck Institute for Dynamics and Self-Organization in Göttingen have discovered that certain areas of the brain generate less information when under anesthesia. The drop in information transfer often measured when the brain is under anesthesia could be a consequence of this reduced local information generation and not – as was so far assumed – a result of disrupted signal transmission between brain areas.
If only a few telephone calls are made in a city then it could be the case that several telecommunication systems have broken down – or it is nighttime and most people are asleep. The situation is similar in an anesthetized brain: if there is remarkably little information transfer between various areas of the brain then either signal transmission in the nerve fibers is blocked or certain areas of the brain are less active as far as the generation of information is concerned.
Patricia Wollstadt, Favio Frohlich, their colleagues from the Brain Imaging Center at Goethe University Frankfurt and researchers at the MPI for Dynamics and Self-Organization have investigated this second hypothesis. Scientists used ferrets to examine “source” brain areas from which less information was transmitted under anesthesia than in a waking state.
They found that information generation under anesthesia was far more affected there than in the “target” brain areas to which the information was transferred. This indicates that it is the information available in the source area which determines information transfer and not a disruption in signal transmission. Were the latter the case, a far greater reduction could be expected in the target areas since less information “arrives” there.
“The relevance of this alternative explanation goes beyond anesthesia research, says Patricia Wollstadt, “since each and every examination of neuronal information transfer should categorically take into consideration how much information is available locally and is therefore also transferable.”
Journal article:
http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005511
Source & further reading:
http://www.goethe-university-frankfurt.de/66934196/019
#neuroscience #anesthesia #research #medicine #consciousness
To date, researchers assumed that anesthetics interrupt signal transmission between different areas of the brain and that is why we lose consciousness. Neuroscientists at Goethe University Frankfurt and the Max Planck Institute for Dynamics and Self-Organization in Göttingen have discovered that certain areas of the brain generate less information when under anesthesia. The drop in information transfer often measured when the brain is under anesthesia could be a consequence of this reduced local information generation and not – as was so far assumed – a result of disrupted signal transmission between brain areas.
If only a few telephone calls are made in a city then it could be the case that several telecommunication systems have broken down – or it is nighttime and most people are asleep. The situation is similar in an anesthetized brain: if there is remarkably little information transfer between various areas of the brain then either signal transmission in the nerve fibers is blocked or certain areas of the brain are less active as far as the generation of information is concerned.
Patricia Wollstadt, Favio Frohlich, their colleagues from the Brain Imaging Center at Goethe University Frankfurt and researchers at the MPI for Dynamics and Self-Organization have investigated this second hypothesis. Scientists used ferrets to examine “source” brain areas from which less information was transmitted under anesthesia than in a waking state.
They found that information generation under anesthesia was far more affected there than in the “target” brain areas to which the information was transferred. This indicates that it is the information available in the source area which determines information transfer and not a disruption in signal transmission. Were the latter the case, a far greater reduction could be expected in the target areas since less information “arrives” there.
“The relevance of this alternative explanation goes beyond anesthesia research, says Patricia Wollstadt, “since each and every examination of neuronal information transfer should categorically take into consideration how much information is available locally and is therefore also transferable.”
Journal article:
http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005511
Source & further reading:
http://www.goethe-university-frankfurt.de/66934196/019
#neuroscience #anesthesia #research #medicine #consciousness
Post has attachment
Distinct wiring mode found in chandelier cells
A basic tenet of neural development is that young neurons make far more connections than they will actually use, with very little specificity. They selectively maintain only the ones that they end up needing. Once many of these connections are made, the brain employs a use-it or lose-it strategy; if the organism’s subsequent experiences stimulate the synapse, it will strengthen and survive. If not, the synapse will weaken and eventually disappear.
Researchers from Hiroki Taniguchi’s lab at the Max Planck Florida Institute for Neuroscience (MPFI) published a study in eNeuro in May 2017 showing for the first time that a unique type of inhibitory interneuron called chandelier cells – which are implicated in several diseases affecting the brain such as schizophrenia and epilepsy – seem to develop their connections differently than other types of neurons.
Neurons have several dendrites – thin protrusions through which they receive input from many other cells, but only one axon, where all the information the cell receives is integrated and sent as a single outgoing signal. Most cells’ axons reach out and form synapses on other cells’ dendrites or cell bodies, but chandelier cells exclusively inhibitory synapse on other cells’ axon initial segments (AIS), right where the cell begins to send its own signal down the axon. At this location, the chandelier cells have a greater impact on other cell’s behavior. “Chandelier cells are the final gatekeeper of the action potential,” said Dr. Taniguchi. “We believe this role makes them an especially important factor in controlling epilepsy, where over-excitement spreads throughout the brain unchecked”.
Using their own recently-developed genetic labeling techniques for tracking these cells in early development in mice, Taniguchi and his team observed that, like most neurons, the cells remodeled their axonal organization through development. They also found excessive axonal varicosities that have been considered morphologically synaptic structures.
To investigate whether these varicosities actually contained synaptic molecules, the team expressed synaptic markers in the chandelier cells using transplantation techniques.
What they found was surprising. Only those varicosities that were associated with the AIS contained synapses – the rest appeared to be empty throughout development. This was also corroborated by their ultrastructures obtained with electron microscopy. These findings provide a big clue to understanding how this important cell type properly wires a unique circuit.
Source & further reading:
https://www.maxplanckflorida.org/news-and-media/news/distinct-wiring-mode-found-in-chandelier-cells/
Journal article:
http://www.eneuro.org/content/4/3/ENEURO.0057-17.2017
Gif: Brain biology by MIT
#neuroscience #medicine #neurons #brain #research #chandeliercells
A basic tenet of neural development is that young neurons make far more connections than they will actually use, with very little specificity. They selectively maintain only the ones that they end up needing. Once many of these connections are made, the brain employs a use-it or lose-it strategy; if the organism’s subsequent experiences stimulate the synapse, it will strengthen and survive. If not, the synapse will weaken and eventually disappear.
Researchers from Hiroki Taniguchi’s lab at the Max Planck Florida Institute for Neuroscience (MPFI) published a study in eNeuro in May 2017 showing for the first time that a unique type of inhibitory interneuron called chandelier cells – which are implicated in several diseases affecting the brain such as schizophrenia and epilepsy – seem to develop their connections differently than other types of neurons.
Neurons have several dendrites – thin protrusions through which they receive input from many other cells, but only one axon, where all the information the cell receives is integrated and sent as a single outgoing signal. Most cells’ axons reach out and form synapses on other cells’ dendrites or cell bodies, but chandelier cells exclusively inhibitory synapse on other cells’ axon initial segments (AIS), right where the cell begins to send its own signal down the axon. At this location, the chandelier cells have a greater impact on other cell’s behavior. “Chandelier cells are the final gatekeeper of the action potential,” said Dr. Taniguchi. “We believe this role makes them an especially important factor in controlling epilepsy, where over-excitement spreads throughout the brain unchecked”.
Using their own recently-developed genetic labeling techniques for tracking these cells in early development in mice, Taniguchi and his team observed that, like most neurons, the cells remodeled their axonal organization through development. They also found excessive axonal varicosities that have been considered morphologically synaptic structures.
To investigate whether these varicosities actually contained synaptic molecules, the team expressed synaptic markers in the chandelier cells using transplantation techniques.
What they found was surprising. Only those varicosities that were associated with the AIS contained synapses – the rest appeared to be empty throughout development. This was also corroborated by their ultrastructures obtained with electron microscopy. These findings provide a big clue to understanding how this important cell type properly wires a unique circuit.
Source & further reading:
https://www.maxplanckflorida.org/news-and-media/news/distinct-wiring-mode-found-in-chandelier-cells/
Journal article:
http://www.eneuro.org/content/4/3/ENEURO.0057-17.2017
Gif: Brain biology by MIT
#neuroscience #medicine #neurons #brain #research #chandeliercells
Wait while more posts are being loaded