Tag Archives: Brain Function

Question?: Rett Syndrome In Boys

Lisa asks…

what is Rett’s syndrome?

admin answers:

What is Rett syndrome?
Rett syndrome is a unique developmental disorder that is first recognized in infancy and seen almost always in girls, but can be rarely seen in boys. It is caused by mutations on the X chromosome on a gene called MECP2. There are more than 200 different mutations found on the MECP2 gene. Most of these mutations are found in eight different “hot spots.” It strikes all racial and ethnic groups, and occurs worldwide in 1 of every 10,000 to 23,000 female births.

Rett syndrome is a developmental disorder. It is not a degenerative disorder. It causes problems in brain function that are responsible for cognitive, sensory, emotional, motor and autonomic function. These can include learning, speech, sensory sensations, mood, movement, breathing, cardiac function, and even chewing, swallowing, and digestion.

Rett syndrome symptoms appear after an early period of apparently normal or near normal development until six to eighteen months of life, when there is a slowing down or stagnation of skills. A period of regression then follows when she loses communication skills and purposeful use of her hands. Soon, stereotyped hand movements such as handwashing, gait disturbances, and slowing of the normal rate of head growth become apparent. Other problems may include seizures and disorganized breathing patterns while she is awake. In the early years, there may be a period of isolation or withdrawal when she is irritable and cries inconsolably. Over time, motor problems may increase, but in general, irritability lessens and eye contact and communication improve.

Rett syndrome is confirmed with a simple blood test to identify the MECP2 mutation. However, since the MECP2 mutation is also seen in other disorders, the presence of the MECP2 mutation in itself is not enough for the diagnosis of Rett syndrome. Diagnosis requires either the presence of the mutation (a molecular diagnosis) or fulfillment of the diagnostic criteria (a clinical diagnosis, based on signs and symptoms that you can observe) or both.

Rett syndrome can present with a wide range of disability ranging from mild to severe. The course and severity of Rett syndrome is determined by the location, type and severity of her mutation and X-inactivation. Therefore, two girls of the same age with the same mutation can appear quite different.

Rett syndrome presents many challenges, but with love, therapy and assistance, those with the syndrome can benefit from school and community activities well into middle age and beyond. They experience a full range of emotions and show their engaging personalities as they take part in social, educational, and recreational activities at home and in the community.
Http://www.rettsyndrome.org/index.php?option=com_content&task=view&id=16&Itemid=1000

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Question?: Rett Syndrome Causes

Michael asks…

what is some current research for rett syndrome?

i’m writing it in my brochure and i can’t find it anywhere!

admin answers:

Here are some great facts! Brochures are great when they are loaded with lots of facts and graphics. Use some of these:

Rett syndrome is a unique developmental disorder that is first recognized in infancy and seen almost always in girls, but can be rarely seen in boys.

Rett syndrome has been most often misdiagnosed as autism, cerebral palsy, or non-specific developmental delay

Rett syndrome is caused by mutations on the X chromosome on a gene called MECP2. There are more than 200 different mutations found on the MECP2 gene. Most of these mutations are found in eight different “hot spots.”

Rett syndrome strikes all racial and ethnic groups, and occurs worldwide in 1 of every 10,000 to 23,000 female births.

Rett syndrome is a developmental disorder. It is not a degenerative disorder.

Rett syndrome causes problems in brain function that are responsible for cognitive, sensory, emotional, motor and autonomic function. These can include learning, speech, sensory sensations, mood, movement, breathing, cardiac function, and even chewing, swallowing, and digestion.

Rett syndrome symptoms appear after an early period of apparently normal or near normal development until six to eighteen months of life, when there is a slowing down or stagnation of skills. A period of regression then follows when she loses communication skills and purposeful use of her hands. Soon, stereotyped hand movements such as handwashing, gait disturbances, and slowing of the normal rate of head growth become apparent. Other problems may include seizures and disorganized breathing patterns while she is awake. In the early years, there may be a period of isolation or withdrawal when she is irritable and cries inconsolably. Over time, motor problems may increase, but in general, irritability lessens and eye contact and communication improve.

Rett syndrome is confirmed with a simple blood test to identify the MECP2 mutation. However, since the MECP2 mutation is also seen in other disorders, the presence of the MECP2 mutation in itself is not enough for the diagnosis of Rett syndrome. Diagnosis requires either the presence of the mutation (a molecular diagnosis) or fulfillment of the diagnostic criteria (a clinical diagnosis, based on signs and symptoms that you can observe) or both.

Rett syndrome can present with a wide range of disability ranging from mild to severe. The course and severity of Rett syndrome is determined by the location, type and severity of her mutation and X-inactivation. Therefore, two girls of the same age with the same mutation can appear quite different.

Rett syndrome presents many challenges, but with love, therapy and assistance, those with the syndrome can benefit from school and community activities well into middle age and beyond. They experience a full range of emotions and show their engaging personalities as they take part in social, educational, and recreational activities at home and in the community.

Good luck in your work! 🙂

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Question?: Autism Symptoms In 7 Year Old

Linda asks…

my girlfriends daughter was diagnosed with autism?

what does it mean is it a serious condition? what are the consequences? her daughter is 7 years old

admin answers:

The autism-spectrum disorders encompass a wide range of symptoms, from social awkwardness to a complete inability to interact and communicate. The definition of Autism is a severe disorder of brain function marked by problems with social contact, intelligence and language, together with ritualistic or compulsive behavior and bizarre responses to the environment.

Autism is a lifelong disorder that interferes with the ability to understand what is seen, heard, and touched. This can cause profound problems in personal behavior and in the ability to relate to others. A person with autism must learn how to communicate normally and how to relate to people, objects and events. However, not all patients suffer the same degree of impairment. There is a full spectrum of symptoms, which can range from mild to severe.

Autism occurs in as many as one or two per 1,000 children. It is found four times more often in boys (usually the first-born) and occurs around the world in all races and social backgrounds. Autism usually is evident in the first three years of life, although in some children it’s hard to tell when the problem develops. Sometimes the condition isn’t diagnosed until the child enters school.

While a person with autism can have symptoms ranging from mild to severe, about 10% have an extraordinary ability in one area, such as in mathematics, memory, music, or art. Such children are known as “autistic savants” (formerly known as “idiot savants.”).

The very fact that your girlfriend’s daughter wasn’t diagnosed until the age of 7, makes me think that she has a very mild form of this syndrome. Great strides have been made in the treatment of Autism. Be as supportive as you can to your girlfriend and her daughter. The best to you all.

P.S. I would also seek a second opinion.

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Unreliable Neural Responses Found In Autistic Adults

Main Category: Autism
Article Date: 21 Sep 2012 – 0:00 PDT Current ratings for:
Unreliable Neural Responses Found In Autistic Adults
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Autism is a disorder well known for its complex changes in behavior – including repeating actions over and over and having difficulty with social interactions and language. Current approaches to understanding what causes these atypical behaviors focus primarily on specific brain regions associated with these specific behaviors without necessarily linking back to fundamental properties of the brain’s signaling abilities.

New research led by Carnegie Mellon University neuroscientists takes the first step toward deciphering the connection between general brain function and the emergent behavioral patterns in autism. Published in the journal Neuron, the study shows that autistic adults have unreliable neural sensory responses to visual, auditory and somatosensory, or touch, stimuli. This poor response reliability appears to be a fundamental neural characteristic of autism.

“Within the autism research community, most researchers are looking for the location in the brain where autism happens,” said Ilan Dinstein, a postdoctoral researcher in Carnegie Mellon’s Department of Psychology and lead author of the study. “We’re taking a different approach and thinking about how a general characteristic of the brain could be different in autism – and how that might lead to behavioral changes.”

For the study, 14 adults with autism and 14 without – all between the ages of 19 and 39 – completed sensory experiments while inside a functional magnetic resonance imaging (fMRI) machine located at CMU’s Scientific Imaging and Brain Research center. To test the visual system’s neural response, participants were shown a pattern of moving dots. The auditory stimulation consisted of pure tones presented to both ears, and short air puffs were used to stimulate the somatosensory senses. The fMRI measured each individual’s brain activity during the experiments.

In all of the primary cortices, visual, auditory and somatosensory, the within-individual response reliability was significantly lower – by 30-40 percent – in autism; meaning, there was not a typical, predictable response from trial to trial. Thus, in the individuals with autism, there was significant intra-individual variability, with responses varying from strong to weak. Non-autistic adults had replicable and consistent responses from trial to trial.

“This suggests that there is something very fundamental that is altered in the cortical responses in individual’s with autism,” said Marlene Behrmann, professor of psychology at CMU and a leading expert on using brain imaging to understand autism. “It also begins to build a bridge between the kind of genetic changes that might have given rise to autism in the first place – and the kind of changes in the brain that are responsible for autistic behavioral patterns.

“And, what I think is so powerful is that we sampled visual, auditory and somatosensory senses. We were unbelievably thorough and attacked every sensory modality and showed the same pattern of unreliability across all three senses.”

The study also presents the first time that researchers have investigated multiple sensory systems – at a primary brain function level – within the same autistic individual.

“One of the problems with autism is that there is considerable variability in symptoms across individuals,” Dinstein said. “In this case, we have a tremendous amount of data on each individual and each of their three sensory systems. And, we see the same unreliability across all of them in autism relative to the controls.”

While this study focused on adults, the team plans on taking the research further to study how the details of sensory unreliability play out in younger autistic groups.

“We are not suggesting that unreliable sensory – visual, auditory, touch – responses cause autism,” said David Heeger, professor of psychology and neural science at New York University. “But rather that autism might be a consequence of unreliable activity throughout the brain during development. We’ve measured it in sensory areas of the brain but we hypothesize that the same kind of unreliability might be what’s limiting the development of social and language abilities in the brain areas that subserve those functions.”

In addition to expanding autism research to determine when and how basic neural processing affects autism, the research may have clinical implications.

“The poor cortical response reliability observed in the individuals with autism in this study may represent a biomarker which could contribute to better define Autism Spectrum Disorder (ASD) subtypes,” said Pauline Chaste, a visiting research scholar at the University of Pittsburgh Medical Center who was not affiliated with the research but studies how genetic mutations affect psychiatric disorders. “This is very important because of the great heterogeneity of phenotype in ASD which makes the definition of subphenotypes critical for genetic studies as well as for treatment studies. Thus, the use of this biomarker may help to define new targets for treatment but also to assess efficacy. Moreover this study brings new insight into understanding atypical sensory sensitivity in autism, which is a major concern for a vast majority of patients and remains sorely underexplored.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Lauren Lorenzi, a research associate at Carnegie Mellon, Nancy Minshew from the Department of Neurology at the University of Pittsburgh and Rafael Malach, the Morris and Barbara Levinson Professor of Brain Research at the Weizmann Institute of Science, were also part of the research team.
The Simons Foundation, Pennsylvania Department of Health and the National Institute of Health and National Institute of Child and Human Development’s Autism Center of Excellence at the University of Pittsburgh funded this research.
This study will appear as the cover story of the October 2012 print issue of Neuron. The issue’s cover design was created by Carnegie Mellon’s Communication Design team.
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Learning Disabilities In Kids May Be Preventable With Cancer Drug

Editor’s Choice
Main Category: Pediatrics / Children’s Health
Also Included In: Genetics;  Autism
Article Date: 29 Aug 2012 – 13:00 PDT Current ratings for:
Learning Disabilities In Kids May Be Preventable With Cancer Drug
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According to a new study conducted by researchers at University of Michigan Medical School and published in the journal Cell, a drug which was originally formulated to stop cancer growth may be capable of halting abnormal brain cells from growing in childrens’ brains – which could reduce the risk of learning disabilities.

This new evidence has researchers wondering if anti-tumor drugs could possibly protect kid’s brain who have neurofibromatosis 1 and other learning disabilities during the key developmental stage.

Neurofibromatosis 1 (NF1) is present in 1 in every 3,000 kids. This disease causes tumors to grow all over the children’s bodies, and sometimes results in abnormally large heads, as well as other health problems. Children affected by NF1 have a hard time writing, solving math problems, reading, and behaving appropriately.

Brown marks on skin appear early on if NF1 is present, and doctors often mistake them for birthmarks. The influence on healthy brain function is the most serious problem associated with NF1, and is usually prevalent soon after the brown marks appear. The authors note that the actual impact that NF1 has on brain function is still unknown, regardless of the fact that multiple studies have been done on the tumors that pop up later in the patient’s life.

For their new study, the University of Michigan Medical School researchers analyzed neural stem cells. These are master cells which can transform into different types of neural tissue.

They discovered that the baby mice that had 2 copies of the mutation that results in NF1, had neural stem cells which produced more nerve cells called glia, and did not produce enough neurons – important for the brain and body to communicate with one another.

These mice were treated with a drug called PD0325901, an experimental drug which has been used in trials for treating advanced cancer. This medication targets the actions of cells named MEK/ERK pathway, part of the class of MEK inhibitor drugs.

The scientists found a large difference between the mice with the NF1 mutation that received the medication right from birth – with those mice forming normal brain development. On the other hand, the mice who did not seem to be “normal” when they were first born, but it was noticeable in a couple of days that they were developing abnormally. They were bent over and “scruffy”.

Lead author of the research and an associate professor of internal medicine in the Division of Molecular Medicine and Genetics and in the Department of Cell & Developmental Biology, Yuan Zhu, Ph.D notes that not all children who have been diagnosed with NF1 will benefit from this specific drug, however, other MEK inhibitors are in the process of being made to fight against cancer.

He says:

“The important thing is that we have shown that by treating during this brief window of time early in life, when neural stem cells in a developing brain still have time to ‘decide’ what kind of cell to become, we can cause a lasting effect on neural development.”

The experiment did not involve the scientists analyzing how the mice behaved, learned or what their chances were of developing the benign brain tumors that often come with NF1.

The best way for the drug to work, according to Zhu, is to administer it at the first sign of benign tumors or delay in development, and after toddlers or infants are diagnosed with NF1.

Around 50% of cases of NF1 are due to genetics, where parents have passed down the mutation to their offspring. The other half of NF1 cases develop in the womb by an unknown cause.

Every case of this disease is different. One child might, with parents who have NF1, have very mild symptoms, while at the same time, their brother or sister is struggling with harsh symptoms.

Another form of NF1 is when a “double hit” occurs. These people have 2 copies of the mutated gene in their cells. If an individual has these 2 copies, they tend to suffer from severe learning symptoms and usually have a larger corpus callosum, the part of the body that joins the two halves of the brain and is home to many glia cells, the cells which the mice had many of.

The recent findings make the scientists hopeful that they can use this information to someday help individuals who have genetic problems similar to NF1 and affect the same cell-signaling pathway named RAS. These types of genetic conditions, called “RASopathies” or neuro-cardio-facial-cutaneous (NCFC) syndromes, include Leguis syndrome, Leopard syndrome, Noonan syndrome and Costello syndrome. They are similar to NF1 because they target the face, head, circulation system, and brain.

The gene for NF1 was found late in the 1980s by U-M Medical School faculty member Francis Collins, M.D., Ph.D., and because of his discovery, children with NF1 can be diagnosed effectively and be treated accordingly.

Written by Christine Kearney
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our pediatrics / children’s health section for the latest news on this subject. “ERK Inhibition Rescues Defects in Fate Specification of Nf1-Deficient Neural Progenitors and Brain Abnormalities”
Yuan Wang, Edward Kim, Xiaojing Wang, Bennett G. Novitch, Kazuaki Yoshikawa, Long-Sheng Chang, Yuan Zhu
Cell, August 2012, doi: 10.1016/j.cell.2012.06.034 Please use one of the following formats to cite this article in your essay, paper or report:

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Study Of Brain Development Reveals Brain Stem Cells That May Be Responsible For Higher Functions, Bigger Brains

Main Category: Schizophrenia
Also Included In: Stem Cell Research;  Autism;  Neurology / Neuroscience
Article Date: 11 Aug 2012 – 0:00 PDT Current ratings for:
Study Of Brain Development Reveals Brain Stem Cells That May Be Responsible For Higher Functions, Bigger Brains
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Scientists from The Scripps Research Institute have identified a new stem cell population that may be responsible for giving birth to the neurons responsible for higher thinking. The finding also paves the way for scientists to produce these neurons in culture – a first step in developing better treatments for cognitive disorders, such as schizophrenia and autism, which result from disrupted connections among these brain cells.

Published in the journal Science, the new research reveals how neurons in the uppermost layers of the cerebral cortex form during embryonic brain development.

“The cerebral cortex is the seat of higher brain function, where information gets integrated and where we form memories and consciousness,” said the study’s senior author Ulrich Mueller, a professor and director of the Dorris Neuroscience Center at Scripps Research. “If we want to understand who we are, we need to understand this area where everything comes together and forms our impression of the world.”

In the new study, Mueller’s team identified a neural stem cell in mice that specifically gives rise to the neurons that make up the upper layers of the cerebral cortex. Previously, it was thought that all cortical neurons – those making up both the lower and upper layers – came from the same type of stem cell, called a radial glial cell, or RGC. A neuron’s fate was thought to be determined by the timing of its birth date. The Scripps Research team, however, showed that there is a distinct stem cell progenitor that gives rise to upper layer neurons, regardless of birth date or place.

“Advanced functions like consciousness, thought, and creativity require a lot of different neuronal cell types and a central question has been how all this diversity is produced in the cortex,” said Santos Franco, a senior research associate in Mueller’s laboratory and first author of the paper. “Our study shows this diversity already exists in the progenitor cells.”

Peeling Back the Onion Layers

In mammals, the cortex is made up of six distinct anatomic layers holding different types of excitatory neurons. They are not the uniform layers of a cake, but rather, they are more like the layers wrapped around an onion. The smaller lower layers, on the inside, host neurons that connect to the brain stem and spinal cord to help regulate essential functions such as breathing and movement. The larger upper layers, closer to the outer surface of the brain, contain neurons that integrate information coming in from the senses and connect across the two halves of the brain.

The upper layers are a “relatively young invention,” evolutionarily speaking, having been greatly expanded during primate evolution, said Mueller. They give humans in particular the unique abilities to think abstractly, plan for the future and problem-solve.

For the last two decades, scientists have believed that the fate of cerebral cortex neurons was determined by their birth date because each layer is formed in a time-dependent manner. The lower layer neurons form in the center of the “ball” first, and then the cells that will become the upper layers form last, migrating through the lower layers.

“So the model was that there is a stem cell in the center of the ball that generates the different types of neurons in successive waves,” said Mueller. “What we now show is that there are at least two different populations of RGCs and potentially more.”

Following Fate

Franco first created a line of mice in which he could track upper-layer neurons as they were born and migrated. The team followed a marker gene called Cux2, which was previously reported to be expressed only by upper-layer neurons. By linking a gene for an enzyme called Cre to the Cux2 gene, the scientists could watch any cell expressing Cux2 under the microscope, because the Cre enzyme flips on another gene that glows fluorescent red.

Surprisingly, the team observed Cux2 already turned on in some of the RGCs, even at the earliest points in brain development – embryonic day nine or ten – before any upper-layer neurons exist. Following this population of glowing stem cells through development, the team showed that the cells almost exclusively generated upper-layer neurons. In contrast, the subgroup of RGCs not expressing Cux2 became lower-layer neurons.

Next, the team removed these Cux2-positive precursor cells from their niche in the embryonic brain to see how they would develop in a lab dish. When they cultured both types of RGCs, again only Cux2-expressing RGCs developed into upper-layer neurons.

In developing brains, these Cux2-positive stem cells first self-renew and proliferate before differentiating later into neurons. So, the team wanted to know if a neuron’s birth date determined its fate. To test this, the researchers delivered a TCF4 molecule in utero that forced the Cux2-positive RGCs to prematurely differentiate. Even though it was too early in normal development, the Cux2-positive RGCs still produced upper-layer neurons.

In other words, regardless of position or timing, the Cux2-positive RGCs are destined to become upper-layer neurons. Mueller and colleagues concluded that these stem cells have some intrinsic property that determines their fate from the start.

The work also shows that this RGC subset is responsible for the huge proliferation of cells necessary to create the larger upper-layer cortex found in primate brains. “If we want to understand how the human brain evolved, how we are different from an amphibian, then this one precursor cell may have been important,” said Mueller.

But, bigger brains came with a risk, making humans more prone to disorders when upper-layer neurons don’t form connections properly. Up until now, researchers trying to reproduce human cortical neurons in the lab from stem cells have only generated lower-layer-type neurons. “This opens a door now to try to make the upper-layer neurons, which are frequently affected in psychiatric disorders,” said Mueller.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our schizophrenia section for the latest news on this subject. In addition to Mueller and Franco, authors of the paper, “Fate-restricted neural progenitors in the mammalian cerebral cortex,” were Cristina Gil-Sanz, Isabel Martinez-Garay, Ana Espinosa, Sarah R. Harkins-Perry, and Cynthia Ramos of Scripps Research. Martinez-Garay is now at the University of Oxford.
This research was supported by the Dorris Neuroscience Center, US National Institutes of Health (grant award numbers NS060355, NS046456, MH078833), and California Institute for Regenerative Medicine, and conducted in affiliation with the NIH Blueprint-funded Cre Driver Network.
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Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits

Main Category: Autism
Article Date: 21 May 2012 – 0:00 PDT Current ratings for:
‘Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits’
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Preliminary results from an ongoing, large-scale study by Yale School of Medicine researchers shows that oxytocin – a naturally occurring substance produced in the brain and throughout the body – increased brain function in regions that are known to process social information in children and adolescents with autism spectrum disorders (ASD).

A Yale Child Study Center research team that includes postdoctoral fellow Ilanit Gordon and Kevin Pelphrey, the Harris Associate Professor of Child Psychiatry and Psychology, presented the results at the International Meeting for Autism Research.

“Our findings provide the first, critical steps toward devising more effective treatments for the core social deficits in autism, which may involve a combination of clinical interventions with an administration of oxytocin,” said Gordon. “Such a treatment approach will fundamentally improve our understanding of autism and its treatment.”

Social-communicative dysfunctions are a core characteristic of autism, a neurodevelopmental disorder that can have an enormous emotional and financial burden on the affected individual, their families, and society.

Gordon said that while a great deal of progress has been made in the field of autism research, there remain few effective treatments and none that directly target the core social dysfunction. Oxytocin has recently received attention for its involvement in regulating social abilities because of its role in many aspects of social behavior and social cognition in humans and other species.

To assess the impact of oxytocin on the brain function, Gordon and her team conducted a first-of-its-kind, double-blind, placebo-controlled study on children and adolescents aged 7 to 18 with ASD. The team members gave the children a single dose of oxytocin in a nasal spray and used functional magnetic resonance brain imaging to observe its effect.

The team found that oxytocin increased activations in brain regions known to process social information. Gordon said these brain activations were linked to tasks involving multiple social information processing routes, such as seeing, hearing, and processing information relevant to understanding other people.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. Other authors on the study include Randi H. Bennett, Brent C. vander Wyk, James F. Leckman, and Ruth Feldman.
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‘Finding That Oxytocin Improves Brain Function In Children With Autism Could Lead To Treatment For Associated Social Deficits’

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Mechanism May Aid Treatment For Alzheimer’s And Neurological Disorders Associated With Gamma-Wave Alterations And Cognitive Impairments

Main Category: Alzheimer’s / Dementia
Also Included In: Epilepsy;  Autism
Article Date: 29 Apr 2012 – 0:00 PDT

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Scientists at the Gladstone Institutes have unraveled a process by which depletion of a specific protein in the brain contributes to the memory problems associated with Alzheimer’s disease. These findings provide new insights into the disease’s development and may lead to new therapies that could benefit the millions of people worldwide suffering from Alzheimer’s and other devastating neurological disorders.

The study, led by Gladstone Investigator Jorge J. Palop, PhD, revealed that low levels of a protein, called Nav1.1, disrupt the electrical activity between brain cells. Such activity is crucial for healthy brain function and memory. Indeed, the researchers found that restoring Nav1.1 levels in mice that were genetically modified to mimic key aspects of Alzheimer’s disease (AD-mice) improved learning and memory functions and increased their lifespan. They report their findings in Cell, available online.

“It is estimated that more than 30 million people worldwide suffer from Alzheimer’s disease and that number is expected to rise dramatically in the near future,” said Lennart Mucke, MD, who directs neurological research at Gladstone, an independent and nonprofit biomedical-research organization. “This research improves our understanding of the biological processes that underlie cognitive dysfunction in this disease and could open the door for new therapeutic interventions.”

The researchers’ findings suggest that Nav1.1 levels in special regulatory nerve cells called parvalbumin cells, or PV cells, are essential to generate healthy brain-wave activity – and that problems in this process contribute to cognitive decline in AD-mice and possibly in patients with Alzheimer’s.

In the brain, neurons form highly interconnected networks, using chemical and electrical signals to communicate with each other. The researchers investigated whether this communication between neurons is disrupted in AD-mice, and if so, how this may affect the symptoms of Alzheimer’s disease.

To study this, they performed electroencephalogram (EEG) recordings – a technique that detects abnormalities in the brain’s electrical waves such as those found in patients with epilepsy. They found that similar abnormalities emerged during periods of reduced gamma-wave oscillations – a type of brain wave that is crucial to regulating learning and memory.

“Like a conductor in an orchestra, PV cells regulate brain rhythms by precisely controlling excitatory brain activity,” said Laure Verret, PhD, postdoctoral fellow and lead author. “We found that PV cells in patients with Alzheimer’s and in AD-mice have low levels of the protein Nav1.1 – likely contributing to PV cell dysfunction. As a consequence, AD-mice had abnormal brain rhythms. By restoring Nav1.1 levels, we were able to re-establish normal brain function.”

Indeed, the scientists found that increasing Nav1.1 levels in PV cells improves brain wave activity, learning, memory and survival rates in AD-mice.

“Enhancing Nav1.1 activity, and consequently improving PV cell function, may help in the treatment of Alzheimer’s disease and other neurological disorders associated with gamma-wave alterations and cognitive impairments such as epilepsy, autism and schizophrenia,” said Dr. Palop, who is also an assistant professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. “These findings may allow us to develop therapies to help patients with these devastating diseases.”

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our alzheimer’s / dementia section for the latest news on this subject. Other scientists who participated in this research at Gladstone include Giao Hang, PhD, Kaitlyn Ho, Nino Devidze, PhD, and Anatol Kreitzer, PhD. Funding was provided by a variety of sources, including the National Institutes of Health, the Stephen D. Bechtel, Jr. Foundation, the Philippe Foundation and the Pew and McKnight Foundations.
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Gladstone Institutes. (2012, April 29). “Mechanism May Aid Treatment For Alzheimer’s And Neurological Disorders Associated With Gamma-Wave Alterations And Cognitive Impairments.” Medical News Today. Retrieved from
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posted by Bettina Buzzi on 30 Apr 2012 at 1:53 am

Why not normalize the brain wave activity of the brain waves with the help of neuroptimal or neurofeedback? A most successful treatment without any side effects. I am always amazed at the ignorance of brain scientists and medical staff in this regard

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‘Mechanism May Aid Treatment For Alzheimer’s And Neurological Disorders Associated With Gamma-Wave Alterations And Cognitive Impairments’

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Augmented Brain Functionality With Hyperbaric Oxygen Therapy

The human brain is like a super computer. With complex components, they are the processing unit ensuring that the human body works to its optimum level. The scientists are still amazed at the functionality of this organ and there is always an ongoing research to discover the full potential of the brain. But when the brain is damaged, and results in some parts being dead, it directly undermines some operative function rendering the part inefficient. This is the reason that the people select all possible methods to heal faster.

The human brain can be affected due to many reasons. Some may be genetic like that of autism, cerebral palsy or the Alzheimer’s disease, some may be accidental and some may not have any explanation at all. This is the reason that people wish for the brain to function as it does for the other normal beings. Out of varied neurological treatments available in the market, the hyperbaric oxygen therapy is one of them.

The Hyperbaric Oxygen Therapy has its roots as the treatment for decompression. But later when researched, it was found that hyperbaric oxygen therapy had other significant uses. It could cure gas gangrene, reduce the carbon monoxide toxicity, eradicate carbon dioxide poisoning and showed improved differences in the autistic children. So what is really hyperbaric oxygen therapy? Hyperbaric means in higher pressure. The person is introduced into chambers which have oxygen at higher pressure. The oxygen dissolves in the blood more than normal, increasing the flow of oxygen even in the dead parts of the brain. This therapy has been found to show a marked improvement in patients suffering from the disorders of the nervous system. This therapy ensures that there is increased blood flow in the affected areas. The higher oxygen content once being introduced into the tissues increases the healing process. The very first symptom of the improvement is the increased brain function and thereby leads to the rapid progression of the other relevant brain functions.

Some smile, some wave, some converse, and some feel euphoric after the treatment. When the complex central nervous system is acquainted with an oxygen rich environment, it starts the recovery process. There are the behavioral changes also. The oxygen aids in regaining the dead neurons and thus starts the healing process. The brain perceives the most in the oxygen rich atmosphere, but all other body parts also partake in the therapeutic healing of the body.

Some people choose the hyperbaric centers for the sessions. These usually come with the latest advanced chambers that provide the best of the facilities. Medical personnel monitor the entire process so that any discomfort can be treated immediately. These centers are equipped with state-of-art amenities to help ensure a comfortable session. Some people purchase these chambers especially if they require frequent treatment sessions.

Allen Wood evaluates the importance of treatment via the hyperbaric oxygen therapy for the autistic children. She has found that those undergoing these sessions in a Hyperbaric Centers or at home, to have shown marked improvement in the brain functionality and the behavior.

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Unlocking Autism’s Mysteries: Predicting Autistic Brain Activity And Behavior

Main Category: Autism
Also Included In: Alzheimer’s / Dementia;  IT / Internet / E-mail
Article Date: 08 Mar 2012 – 1:00 PST

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New research from Carnegie Mellon University’s Marcel Just provides an explanation for some of autism’s mysteries – from social and communication disorders to restricted interests – and gives scientists clear targets for developing intervention and treatment therapies.

Autism has long been a scientific enigma, mainly due to its diverse and seemingly unrelated symptoms until now.

Published in the journal Neuroscience and Biobehavioral Reviews, Just and his team used brain imaging and computer modeling to show how the brain’s white matter tracts – the cabling that connects separated brain areas – are altered in autism and how these alterations can affect brain function and behavior. The deficiencies affect the tracts’ bandwidth – the speed and rate at which information can travel along the pathways.

“White matter is the unsung hero of the human brain,” said Just, the D.O. Hebb Professor of Psychology within CMU’s Dietrich College of Humanities and Social Sciences and director of the university’s Center for Cognitive Brain Imaging. “In autistic individuals, we can measure the quality of the white matter, and our computer model can predict how coordinated their brain activity will be. This gives us a precise account of the underlying alterations affecting autistic thought.”

These findings build on Just’s 2004 influential “Frontal-Posterior Underconnectivity Theory of Autism,” which first discovered and explained that the synchronization of the activation between frontal and posterior brain areas is lower in autism. Since then, Just and his team have used more advanced imaging technologies, particularly diffusion imaging of white matter and sophisticated computer models to uncover that the white matter is also altered in autism. Using their computer model, they can relate the poorer quality of the white matter – connecting frontal and posterior brain areas – to the poorer synchronization in the frontal and posterior areas in individual people with autism.

The computer model is able to solve some visual puzzles called the Tower of London (used in neuropsychological testing of frontal lobe function) through the coordinated activity of several computational systems that correspond to frontal and posterior brain areas. The model makes it possible to manipulate the communication bandwidth between the frontal and posterior areas. The findings were that the inter-regional synchronization of activation in a particular individual’s brain could be predicted by calibrating the model’s frontal-posterior communication bandwidth to the quality of that individual’s white matter. Furthermore, the autism model solved the problems by relying less on frontal executive functioning and more on posterior “visual thinking.”

“The brain’s processing of social information is performed by a network of areas, some of which are frontal, and some of which are posterior,” Just explained. “Social impairments in autism are likely caused by the poor frontal-posterior connectivity. Similarly, language comprehension is performed by a network of frontal and posterior areas, and once again, poor connectivity may impair that network’s functioning.”

Just added, “This tells us where the problem lies in autism. We can now focus on designing therapies that attempt to either improve the white matter – something we have already proven is possible through behavioral interventions – or help the brain develop work-around strategies.”

In a groundbreaking study published in 2009, Just and his colleagues showed for the first time that compromised white matter in children with reading difficulties could be repaired with extensive behavioral therapy. Their imaging study showed that the brain locations that had been abnormal prior to the remedial training improved to normal levels after the training, and the reading performance in individual children improved by an amount that corresponded to the amount of white matter change.

“This new research and model makes way for modifying people’s brains and possibly helping people with autism. It also points at the likely source of autism,” Just said.

In addition to autism, these findings also have implications for a number of other psychiatric illnesses that involve white matter deficiencies, such as schizophrenia and Alzheimer’s disease, providing a way to relate the anatomical deficiencies to thought processes.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our autism section for the latest news on this subject. The Autism Centers of Excellence, National Institute of Child Health and Human Development and the Office of Naval Research funded this research.
For more information on this study and where leading cognitive neuroscientist Marcel Just sees this research going in the immediate future, watch this video: http://youtu.be/eSR94zW8mrA.
Carnegie Mellon University Please use one of the following formats to cite this article in your essay, paper or report:

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Carnegie Mellon University. “Unlocking Autism’s Mysteries: Predicting Autistic Brain Activity And Behavior.” Medical News Today. MediLexicon, Intl., 8 Mar. 2012. Web.
9 Mar. 2012. APA

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‘Unlocking Autism\’s Mysteries: Predicting Autistic Brain Activity And Behavior’

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