Posts tagged neuroscience

ScienceDaily (May 7, 2012) — Elderly people with pre-diabetes and type 2 diabetes suffer from an accelerated decline in brain size and mental capacity in as little as two years according to new research presented at the joint International Congress of Endocrinology/European Congress of Endocrinology in Florence, Italy. 

An Australian research team led by Associate Professor Katherine Samaras (Garvan Institute of Medical Research) found that the aging brain is vulnerable to worsening blood sugar levels even before type 2 diabetes is diagnosable.

While some brain volume loss is a normal part of aging, the researchers found that elderly people with blood sugar levels in flux, as well as type 2 diabetes, lost almost two and a half times more brain volume than their peers over two years. The reduction in size of the frontal lobe — associated with higher mental functions like decision-making, emotional control, and long term memory — has a significant impact on cognitive function and quality of life.

Diabetes is a very common disorder caused by high levels of sugar in the bloodstream. It affects 6.4% (285 million) of the worldwide population and is associated with an increased risk of heart attacks, stroke and damage to the eyes, feet and kidneys. In type 2 diabetes, which accounts for 90% of all cases, insulin — a hormone that allows cells to take sugar from the bloodstream and store it as energy — does not work properly. 344 million people also have pre-diabetes, a condition with mildly elevated blood sugar levels that gives them a 50% risk of developing the disease over ten years.

This research — a follow-up of 312 participants from the Sydney Memory and Ageing Study — compared MRI scans taken from the beginning and end of a two-year period. The participants were elderly community-dwelling Australians aged between 70 and 90 years old (average age 78, 54% male) and free from dementia. At the start of the study 41% had pre-diabetes and 13% had type 2 diabetes.

At the end of the study the participants were divided into four groups: (1) those with normal, stable glucose levels (102 people); (2) those with stable pre-diabetes (120 people); (3) those whose glucose levels had worsened (57 people); and finally, (4) those with type 2 diabetes from the start (33 people).

The MRI scans showed that the normal group lost an average of 18.4 cm3 total brain volume over two years. In comparison, the stable pre-diabetic group lost 1.4 times more brain volume (26.6 cm3). Both the third group (worsening glucose levels) and fourth group (type 2 diabetes) lost 2.3 times the stable group’s brain volume loss (41.7 cm3 and 42.3 cm3, respectively).

The researchers — using statistical models that accounted for other variables — concluded that a person’s blood sugar status after two years can significantly predict their decline in brain volume.

Associate Professor Katherine Samaras, from the Garvan Institute of Medical Research, said:

"These findings highlight the importance of prevention of diabetes. They also emphasise that, in the elderly, clinicians and allied health professionals need to understand that the complexity of diabetes care needs to accommodate expected declines in cognitive function.

"We need to understand why these changes in cognition and brain size occur. Is it due merely to higher blood sugars? Is the brain subject to the toxic effects of glucose, just as peripheral nerves are? To what extent do other factors associated with diabetes also contribute to the decline in brain size and function, for example inflammation or blood fat levels?

"We also need to learn how we can prevent or deter the negative effects of diabetes on the brain."

Source: Science Daily

ScienceDaily (May 7, 2012) — A Kansas State University graduate student is creating a schoolyard that can become a therapeutic landscape for children with autism.

Chelsey King, master’s student in landscape architecture, St. Peters, Mo., is working with Katie Kingery-Page, assistant professor of landscape architecture, to envision a place where elementary school children with autism could feel comfortable and included.

"My main goal was to provide different opportunities for children with autism to be able to interact in their environment without being segregated from the rest of the school," King said. "I didn’t want that separation to occur."

The schoolyard can be an inviting place for children with autism, King said, if it provides several aspects: clear boundaries, a variety of activities and activity level spaces, places where the child can go when overstimulated, opportunities for a variety of sensory input without being overwhelming and a variety of ways to foster communication between peers.

"The biggest issue with traditional schoolyards is that they are completely open but also busy and crowded in specific areas," King said. "This can be too overstimulating for a person with autism."

King researched ways that she could create an environment where children with autism would be able to interact with their surroundings and their peers, but where they could also get away from overstimulation until they felt more comfortable and could re-enter the activities.

"Through this research, I was able to determine that therapies and activities geared toward sensory stimulation, cognitive development, communication skills, and fine and gross motor skills — which traditionally occur in a classroom setting — could be integrated into the schoolyard," King said.

King designed her schoolyard with both traditional aspects — such as a central play area — and additional elements that would appeal to children with autism, including:

* A music garden where children can play with outdoor musical instruments to help with sensory aspects.

* An edible garden/greenhouse that allows hands-on interaction with nature and opportunities for horticulture therapy.

* A sensory playground, which uses different panels to help children build tolerances to difference sensory stimulation.

* A butterfly garden to encourage nature-oriented learning in a quiet place.

* A variety of alcoves, which provide children with a place to get away when they feel overwhelmed and want to regain control.

King created different signs and pictures boards around these schoolyard elements, so that it was easier for children and teachers to communicate about activities. She also designed a series of small hills around the central play areas so that children with autism could have a place to escape and watch the action around them.

"It is important to make the children feel included in the schoolyard without being overwhelmed," King said. "It helps if they have a place — such as a hill or an alcove — where they can step away from it and then rejoin the activity when they are ready.

King and Kingery-Page see the benefits of this type of schoolyard as an enriching learning environment for all children because it involves building sensory experience and communication.

"Most children spend seven to nine hours per weekday in school settings," Kingery-Page said. "Designing schoolyards that are educational, richly experiential, with potentially restorative nature contact for children should be a community concern."

The researchers collaborated with Jessica Wilkinson, a special education teacher who works with children with autism. King designed her schoolyard around Amanda Arnold Elementary School, which is the Manhattan school district’s magnet school for children with autism.

"Although there are no current plans to construct the schoolyard, designing for a real school allowed Chelsey to test principles synthesized from literature against the actual needs of an educational facility," Kingery-Page said. "Chelsey’s interaction with the school autism coordinator and school principal has grounded her research in the daily challenges of elementary education for students with autism."

Source: Science Daily

May 7, 2012 

(Medical Xpress) — An international study led by the University of Sydney and published in the Annals of Neurology has the potential to improve the design of clinical trials for the treatment of Charcot-Marie-Tooth disease, a disorder which affects the peripheral nervous system.

Charcot-Marie-Tooth disease (CMT) is among the most common inherited neurological disorders, affecting one in 2500 people. Symptoms such as leg weakness, foot pain, trips and falls develop in the first two decades of life, with some patients wheelchair bound by 21 years. Currently there is no treatment for any form of this disease, but clinical trials are increasingly occurring.

"While it is very positive that clinical trials are taking place in this area, it is vital that trials are based on appropriately selected patients and carefully chosen outcome measures," says Associate Professor Joshua Burns, Chief Investigator from the University of Sydney and The Children’s Hospital at Westmead. "This relies on being able to measure disease severity accurately, and in turn the patient’s response to treatment, which we were previously unable to do in children."

In response, Associate Professor Burns and colleagues from the USA, UK and Italy designed the CMT Pediatric Scale (CMTPedS), a patient-centred multi-item rating scale of disability for children with CMT.

"Rating scales used for adult patients are inappropriate for children and since most forms of CMT affect children there was an obvious need for a new clinical tool.

"Furthermore, it is during childhood that we anticipate that treatments for CMT may be most effective - before the disease progresses and makes repair more difficult."

During a 14-month test period the CMTPedS was administered to more than 170 children aged three to 20 with varying types of CMT in Australia and internationally via the Inherited Neuropathies Consortium. Analysis of these data supported the viability of CMTPedS as a reliable, valid and sensitive global measure of disability for children with CMT from the age of three years.

The CMTPedS can be completed in 25 minutes and will have broad application in clinical trials of rehabilitative, pharmacological and surgical interventions.

"There is growing international support for the rating scale to be implemented as the primary outcome measure in studies of children with CMT because the quality of the measure has the potential to influence the outcome of clinical trials and patient care," says Associate Professor Burns.

Provided by University of Sydney

Source: medicalxpress.com

May 7, 2012

Many of us love massages, but imagine a massage so deep that tissues, organs and cells could also be ‘massaged’.

That’s exactly what Vibroacoustic Therapy, a low frequency sound massage, is clinically proven to do, and new research at U of T suggests that it may help people with debilitating diseases.

“It is basically stimulating the body with very low sound – like sitting on a subwoofer,” said Professor Lee Bartel of the Faculty of Music.  “But it requires special speakers that carry sound almost too low to hear in a way that changes it basically to something you feel instead of hear.”

Bartel and his team in the new Music and Health Research Collaboratory (MaHRC) are exploring the medical effects of low frequency sound and have shown that this therapy can play a key role in reducing the symptoms of Parkinson’s disease.

Vibroacoustic therapy (VAT) consists of low sound frequencies that are transmitted to the body and mind through special transducers that convert the sound to inner body massage. MaHRC associates Heidi Ahonen and Quincy Almeida treated two groups of Parkinson’s patients (20 with dominant tremor symptoms and 20 with slow/rigid movement symptoms) with five minutes of 30 Hz vibration.

Both groups showed improvements in all symptoms, including less rigidity and better walking speed with bigger steps and less tremor.

“There have been several studies using vibration from sound with Parkinson’s,” said Bartel   “It has been known for over 100 years that vibration (like riding in a wagon on cobblestones) helped relieve some symptoms. So the scientific study of the effect of low frequency sound was a natural connection. Also known is that 40 Hz brain waves seem to be carriers of information between the parts of the brain that control movement. So adding extra stimulation in that zone should help that communication and so assist in movement control.”

Bartel, Founding and Acting Director of MaHRC, says the goal of low frequency sound studies with Parkinson’s is to determine which approach is most effective, how much and how often treatment is needed, and whether medication can be reduced. Vibroacoustic Therapy frequencies, between 20 and 100 Hz or pulses per second, correspond to brainwave activities and function that are currently being explored in neuroscience. 

But the effects of Vibroacoustic Therapy extend beyond the brain. It also provides deep physical cellular stimulation to skin, muscles and joints, resulting in decreased pain and increased mobility. Like hand/mechanical massage, vibroacoustic therapy aids circulation, relaxes muscles, and feels good.

Bartel points to research that shows that “several medical conditions including Parkinson’s and neuralgic pain like fibromyalgia, may be related to a common brain mechanism – a brain rhythm disorientation between the inner brain and the outer cortex. Since the rhythmic pulses of music can drive and stabilize these, we speculate that low frequency sound might help in fibromyalgia as well as Parkinson’s.”

Bartel’s team is now looking at the role of vibroacoustic therapy as a treatment for patients with fibromyalgia.

“Although it is too early to form any conclusions, there is encouraging data indicating that treating fibromyalgia patients with doses of 40 Hz sound seems to reduce pain.” 

“It is truly an exciting time for music medicine – the idea of developing audioceuticals (prescribable sound) points to a whole new direction for music therapy, and the potential for MaHRC to lead in this is very exciting for me” said Bartel.      

Provided by University of Toronto

Source: medicalxpress.com

May 7, 2012

Erxi Wu, assistant professor of pharmaceutical sciences, and Shuang Zhou, a doctoral student in Wu’s lab, co-wrote the article, “Smilagenin Attenuates Beta Amyloid (25-35)-Induced Degeneration of Neuronal Cells via Stimulating the Gene Expression of Brain-Derived Neurotrophic Factor,” which will be published by Neuroscience. They collaborated with Yaer Hu lab at Shanghai Jiaotong University, China, for the publication.

According to the authors, the development of drugs that weaken neurodegeneration is important for the treatment of Alzheimer’s disease. They previously found that smilagenin, a steroidal sapogenin from traditional Chinese medicinal herbs that improves memory in animal models, is neither a cholinesterase inhibitor nor a glutamate receptor antagonist, but can significantly elevate the declined muscarinic receptor (M receptor density). In this paper, to clarify whether smilagenin represents a new approach for treating neurodegeneration disease, they first demonstrate that smilagenin pretreatment significantly attenuates the neurodegenerative changes induced by beta amyloid 25-35 (Aβ25-35) in cultured rat cortical neurons, including decreased cholinergic neuron number, shortened neurite outgrowth length and declined muscarinic receptor density. Brain-derived neurotrophic factor protein in the culture medium was also decreased by Aβ25-35 and significantly elevated by smilagenin. 

Parallel experiments revealed that when the trk receptors were inhibited by K252a or the action of brain-derived neurotrophic factor was inhibited by a neutralizing anti- brain-derived neurotrophic factor antibody, the effects of smilageninon the Aβ25-35 induced neurodegeneration in rat cortical neurons were almost completely abolished. In the all-trans retinoic acid-differentiated SH-SY5Y neuroblastoma cells, the brain-derived neurotrophic factortranscription rate measured by a nuclear run-on assay was significantly suppressed by Aβ25-35 and elevated by SMI, but the brain-derived neurotrophic factor degradation rate measured by half-life determination was unchanged by Aβ25-35 and smilagenin. Transcript analysis of the SH-SY5Y cells using quantitative RT-PCR showed that the IV and VI transcripts of brain-derived neurotrophic factor mRNA were significantly decreased by Aβ25-35 and elevated by smilagenin. 

“Taken together, this study concludes that smilagenin attenuates Aβ25-35-induced neurodegeneration in cultured rat cortical neurons and SH-SY5Y cells mainly through stimulating brain-derived neurotrophic factor mRNA transcription implicating that SMI may represent a novel therapeutic strategy for Alzheimer’s disease,” Wu said. “Collaborating with Dr. Hu at Shanghai Jiaotong University, China, we together would like to find better therapeutics and elucidate the mechanisms of the potential novel therapy for Alzheimer’s disease,” Wu said.

Provided by North Dakota State University

Source: medicalxpress.com

May 6, 2012

Gaining access to the inner workings of a neuron in the living brain offers a wealth of useful information: its patterns of electrical activity, its shape, even a profile of which genes are turned on at a given moment. However, achieving this entry is such a painstaking task that it is considered an art form; it is so difficult to learn that only a small number of labs in the world practice it.

Researchers at MIT and the Georgia Institute of Technology have developed a way to automate a process called whole-cell patch clamping, which involves bringing a tiny hollow glass pipette in contact with the cell membrane of a neuron, then opening up a small pore in the membrane to record the electrical activity within the cell. Credit: Sputnik Animation and MIT McGovern Institute

But that could soon change: Researchers at MIT and the Georgia Institute of Technology have developed a way to automate the process of finding and recording information from neurons in the living brain. The researchers have shown that a robotic arm guided by a cell-detecting computer algorithm can identify and record from neurons in the living mouse brain with better accuracy and speed than a human experimenter.

The new automated process eliminates the need for months of training and provides long-sought information about living cells’ activities. Using this technique, scientists could classify the thousands of different types of cells in the brain, map how they connect to each other, and figure out how diseased cells differ from normal cells.

The project is a collaboration between the labs of Ed Boyden, associate professor of biological engineering and brain and cognitive sciences at MIT, and Craig Forest, an assistant professor in the George W. Woodruff School of Mechanical Engineering at Georgia Tech.

"Our team has been interdisciplinary from the beginning, and this has enabled us to bring the principles of precision machine design to bear upon the study of the living brain," Forest says. His graduate student, Suhasa Kodandaramaiah, spent the past two years as a visiting student at MIT, and is the lead author of the study, which appears in the May 6 issue of Nature Methods.

The method could be particularly useful in studying brain disorders such as schizophrenia, Parkinson’s disease, autism and epilepsy, Boyden says. “In all these cases, a molecular description of a cell that is integrated with [its] electrical and circuit properties … has remained elusive,” says Boyden, who is a member of MIT’s Media Lab and McGovern Institute for Brain Research. “If we could really describe how diseases change molecules in specific cells within the living brain, it might enable better drug targets to be found.”

Read more …

May 6, 2012 

Brain networks may avoid traffic jams at their busiest intersections by communicating on different frequencies, researchers at Washington University School of Medicine in St. Louis, the University Medical Center at Hamburg-Eppendorf and the University of Tübingen have learned.

"Many neurological and psychiatric conditions are likely to involve problems with signaling in brain networks," says co-author Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology at Washington University. "Examining the temporal structure of brain activity from this perspective may be especially helpful in understanding psychiatric conditions like depression and schizophrenia, where structural markers are scarce."

The research will be published May 6 in Nature Neuroscience.

Scientists usually study brain networks — areas of the brain that regularly work together — using magnetic resonance imaging, which tracks blood flow. They assume that an increase in blood flow to part of the brain indicates increased activity in the brain cells of that region.

"Magnetic resonance imaging is a useful tool, but it does have limitations," Corbetta says. "It only allows us to track brain cell activity indirectly, and it is unable to track activity that occurs at frequencies greater than 0.1 hertz, or once every 10 seconds. We know that some signals in the brain can cycle as high as 500 hertz, or 500 times per second."

For the new study, conducted at the University Medical Center at Hamburg-Eppendorf, the researchers used a technique called magnetoencephalography (MEG) to analyze brain activity in 43 healthy volunteers. MEG detects very small changes in magnetic fields in the brain that are caused by many cells being active at once. It can detect these signals at rates up to 100 hertz.

"We found that different brain networks ticked at different frequencies, like clocks ticking at different speeds," says lead author Joerg Hipp, PhD, of the University Medical Center at Hamburg-Eppendorf and the University of Tübingen, both in Germany.

For example, networks that included the hippocampus, a brain area critical for memory formation, tended to be active at frequencies around 5 hertz. Networks constituting areas involved in the senses and movement were active between 32 hertz and 45 hertz. Many other brain networks were active at frequencies between eight and 32 hertz. These “time-dependent” networks resemble different airline route maps, overlapping but each ticking at a different rate.

"There have been a number of fMRI studies of depression and schizophrenia showing ‘spatial’ changes in the organization of brain networks," Corbettta says. "MEG studies provide a window into a much richer ‘temporal’ structure. In the future, this might offer new diagnostic tests or ways to monitor the efficacy of interventions in these debilitating mental conditions."

Provided by Washington University School of Medicine

Source: medicalxpress.com

ScienceDaily (May 4, 2012) — Researchers in Spain have found that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability.

New research suggests that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability. (Credit: © Nikki Zalewski / Fotolia)

In synesthetes, the brain regions responsible for the processing of each type of sensory stimuli are intensely interconnected. Synesthetes can see or taste a sound, feel a taste, or associate people or letters with a particular color.

The study was conducted by the University of Granada Department of Experimental Psychology Óscar Iborra, Luis Pastor and Emilio Gómez Milán, and has been published in the journal Consciousness and Cognition. This is the first time that a scientific explanation has been provided for the esoteric phenomenon of the aura, a supposed energy field of luminous radiation surrounding a person as a halo, which is imperceptible to most human beings.

In basic neurological terms, synesthesia is thought to be due to cross-wiring in the brain of some people (synesthetes); in other words, synesthetes present more synaptic connections than “normal” people. “These extra connections cause them to automatically establish associations between brain areas that are not normally interconnected,” professor Gómez Milán explains. New research suggests that many healers claiming to see the aura of people might have this condition.

The case of the "Santón de Baza"

One of the University of Granada researchers remarked that “not all ‘healers’ are synesthetes, but there is a higher prevalence of this phenomenon among them. The same occurs among painters and artists, for example.” To carry out this study, the researchers interviewed some synesthetes including a ‘healer’ from Granada, “Esteban Sánchez Casas,” known as"El Santón de Baza".

Many local people attribute “paranormal powers” to El Santón, because of his supposed ability to see the aura of people “but, in fact, it is a clear case of synesthesia,” the researchers explained. According to the researchers, El Santón has face-color synesthesia (the brain region responsible for face recognition is associated with the color-processing region); touch-mirror synesthesia (when the synesthete observes a person who is being touched or is experiencing pain, s/he experiences the same); high empathy (the ability to feel what other person is feeling), and schizotypy (certain personality traits in healthy people involving slight paranoia and delusions). “These capacities make synesthetes have the ability to make people feel understood, and provide them with special emotion and pain reading skills,” the researchers explain.

In the light of the results obtained, the researchers remarked on the significant “placebo effect” that healers have on people, “though some healers really have the ability to see people’s ‘auras’ and feel the pain in others due to synesthesia.” Some healers “have abilities and attitudes that make them believe in their ability to heal other people, but it is actually a case of self-deception, as synesthesia is not an extrasensory power, but a subjective and ‘adorned’ perception of reality,” the researchers state.

Source: Science Daily

May 5, 2012 

In an effort to identify the underlying causes of neurological disorders that impair motor functions such as walking and breathing, UCLA researchers have developed a novel system to measure the communication between stem cell-derived motor neurons and muscle cells in a Petri dish.

The study provides an important proof of principle that functional motor circuits can be created outside of the body using stem cell-derived neurons and muscle cells, and that the level of communication, or synaptic activity, between the cells could be accurately measured by stimulating motor neurons with an electrode and then measuring the transfer of electrical activity into the muscle cells to which the motor neurons are connected.

When motor neurons are stimulated, they release neurotransmitters that depolarize the membranes of muscle cells, allowing the entry of calcium and other ions that cause them to contract. By measuring the strength of this activity, one can get a good estimation of the overall health of motor neurons. That estimation could shed light on a variety of neurodegenerative diseasessuch as spinal muscular atrophy and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, in which the communication between motor neurons and muscle cells is thought to unravel, said study senior author Bennett G. Novitch, an assistant professor of neurobiology and a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The findings of the study appear May 4, 2012 in PLoS ONE, a peer-reviewed journal of the Public Library of Science.

"Now that we have this method to measure the strength of the communications between motor neurons and muscle cells, we may be able to begin exploring what happens in the earliest stages of motor neuron disease, before neuronal death becomes prevalent," Novitch said. "This can help us to pinpoint where things begin to go wrong and provide us with new clues into therapeutic interventions that could improve synaptic communication and promote neuronal survival."

Novitch said the synaptic communication activity his team was able to create and measure using mouse embryonic stem cell-derived motor neurons and muscle cells looks very similar what is seen in a mouse, validating that their model is a realistic representation of what is happening in a living organism.

"That gives us a good starting point to try to model what happens in cells that harbor genetic mutations that are associated with neurodegenerative diseases,. To do that, we had to first define an activity profile of normal synaptic communication," he said. "Some research suggests that a breakdown in this communication can be an early indication of disease progression or possibly an initiating event. Neurons that cannot effectively transmit information to muscle cells will eventually withdraw their contacts, causing both the neurons and muscle cells to degenerate over time. Hopefully, we can now create disease models that will allow us to study what is happening."

In this study, Novitch and his team, led by Joy Umbach, an associate professor of molecular and medical pharmacology, used mouse embryonic stem cells to create the motor neurons and previously established lines of muscle precursors to produce muscle fibers. They put both cells together in a Petri dish, and the cells were cultured in such a way to encourage communication. Novitch said the team wanted to see if they would naturally form synaptic contacts and whether or not there was neural transmission between them.

In less than a week, the neurons had reached out to the muscle cells and assembled the protein networks needed for synaptic communication, Novitch said.

To measure the connections between the cells, the scientists used a technique called dual patch clamp recording. Pipettes containing stimulating and recording electrodes are inserted into the membranes of the motor neurons and muscle cells, being careful not to injure them. With this method, they were able send an electrical current into the motor neurons and measure responses in the muscle cells, as well as visualize the muscular contractions.

"The in vitro system developed here might accordingly be expanded to assess the underlying cellular and molecular mechanisms that contribute to this decline in synaptic input to motor neurons," the study states. "Thus, in addition to their utility for helping to answer fundamental biological questions, these co-cultures have clear applications in addressing problems of medical significance."

Going forward, Novitch and his team hope to recreate and confirm the work using human stem cell-derived motor neurons and muscle cells and measure the synaptic communications with newly developed optical recording methods, which are less invasive than the patch clamp techniques used in this study.

Provided by University of California, Los Angeles

Source: medicalxpress.com

ScienceDaily (May 3, 2012) — Malfunctioning single proteins can cause disruptions in neuronal junctions leading to autistic forms of behavior. A current study, published in the scientific journal Nature, comes to this conclusion after examining genetically altered mice.

The study, in which scientists from Charité — Universitätsmedizin Berlin and the NeuroCure Cluster of Excellence contributed, thus supports the hypothesis that disruptions in neuronal junctions, i.e. synapses, could be the cause of the development of neuropsychiatric illnesses like autism. The international research team, that included scientists from Ulm University and the Institut Pasteur in Paris, ascribes a key role to the excitatory synapses. This finding could become an important step stone for future autism therapies.

Nerve cells communicate with each other via signal transmission to synaptic junctions. These junctions are stabilized through structural proteins, including the so-called ProSAP1/Shank2 protein. In order to understand the role that this protein has on synapses and ultimately in the development of autism, the researchers genetically modified mice and disabled the relevant protein. The choice of this protein was not arbitrary: In preparation for the current study, a number of the scientists involved found evidence that the mutation of this protein can lead to autism in humans. Various neuronal developmental disorders manifested through distinctive social and communicative behavioral features, as well as stereotyped behaviors are combined under the term of “autism.”

The absence of this structural protein in the mouse model also had visible implications: Animals with the mutated gene are hyperactive and demonstrate compulsive repetitions of particular features — like grooming, for example. In behavioral experiments, peculiarities in social and communicative interaction also become distinct. In the brains of the mice, researchers found noticeable mutations of synaptic junctions — specifically in excitatory synapses. When glutamate transmitters bind to glutamate receptors located at these junctions, the nerve cells become excitatory. If the mouse is lacking this structural protein, the transmitters increasingly find a related structural protein on the excitatory synapses, the ProSAP2/Shank3. This protein has also been implicated in the development of autism. At the same time, the composition of glutamate receptors mutates.

But what happens when this related structural protein in the mice is switched off? This is also examined in the study presented. The conclusion is that, in this case as well, mutations of the excitatory synapses occur. Obviously, both structural molecules alternate in fulfilling regular functions. “The study illustrates the significant role glutamatergic systems play in autism and thus contributes to understanding better synaptic changes in autism,” reports Stephanie Wegener, one of the participating scientists at Charité Berlin. The study is therefore an important part of the essential scientific foundation needed to develop possible therapies for autism.

Source: Science Daily