Tag Archives: Plasticity

Question?: Rett Syndrome Research

Chris asks…

Does anyone know why Rett Syndrome girls start off “normal” & then regress?

Okay I’m aware of what Rett Syndrome is & how it works (for the most part anyway) but what has me confused the most is that most of these girls develope normally for about the first 6-18 minths & then start to regress/lose skills they’ve already learned (i.e. talking, walking, eye contact) . I know this is due to a mutation in the MEPc2 gene but why/how is it they can learn things & then lose them later on. I relize the gene is responsible for turning on/off certian protiens but what is making these girls funtion properly in the beginning then? another gene maybe?

admin answers:

To quote a passage from wikipedia:
“The recent studies demonstrating that neurological deficits resulting from loss of MeCP2 can be reversed upon restoration of gene function are quite exciting because they show that neurons that have suffered the consequences of loss of MeCP2 function are poised to regain functionality once MeCP2 is provided gradually and in the correct spatial distribution. This provides hope for restoring neuronal function in patients with RTT. However, the strategy in humans will require providing the critical factors that function downstream of MeCP2 because of the challenges in delivering the correct MeCP2 dosage only to neurons that lack it, given that the slightest perturbation in MeCP2 level is deleterious. Thus, therapeutic strategies necessitate the identification of the molecular mechanisms underlying individual RTT phenotypes and picking out the candidates that can be therapeutically targeted. The next phase of research needs to assess how complete the recovery is. Clearly, lethality, level of activity, and hippocampal plasticity are rescued, but are the animals free of any other RTT symptoms such as social behavior deficits, anxiety, and cognitive impairments? Since postnatal rescue results in viability, it will be important to evaluate if even the subtler phenotypes of RTT and MECP2 disorders are rescued when protein function is restored postnatally. This is particularly important given emerging data about early neonatal experiences and their long-term effects on behavior in adults.”

What I get from that is that the nerves become damaged by the defective gene, resulting in a loss of abilities that have already been learned.

Sorry if you’ve already read this, but this is just about all I could find as far as the reason for the decline period.
Hope this helps!

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Question?: Adhd Lyrics

Steven asks…

If a brain is great at remembering music but not able to remember digits or names as well, how does this work?

Does the brain use up more neurons and cells remembering music (exact tones and pitches) or do names and numbers take up more?

Does anyone really know the answer? We all know that the brain is still an absolute mystery to science. So what are your theories on the above question – seeing as science will probably never know.

admin answers:

The brain is very complex and costly to build during embryogenesis.
Small nutrient disruptions or other stresses can influence critical development points in early growth. Each fetus experiences some degree of growth limiting deficits at different times that influence how it develops from the genetic potential it inherited.

However the brain has a genetic plasticity with many overlapping functions so small local growth perturbations can be compensated for. Later, after birth while the brain continues to grow, learning & experience further alter the patterns of interactive networks that develop and help in compensating for slight growth differences.
Http://social.jrank.org/pages/515/Prenatal-Development-Prenatal-Environmental-Influences.html
http://pediatrics.aappublications.org/cgi/content/full/118/4/1486
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYT-485Y83S-K&_user=10&_coverDate=02%2F29%2F1976&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1423574263&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=60f4e05c49dc10f6b3e817b66cc8a45d

Post natal normal brain development MRI study
http://webcache.googleusercontent.com/search?q=cache:GzDidA8WiQsJ:stbb.nichd.nih.gov/pdf/NIH_MRI_neuropsychological.pdf+MRI+brain+scan+calculations+nouns+memory+center&hl=en&gl=us
The medial pre-frontal cortex is a music-processing region in the brain. MRI scans of test subjects listening to music show this area is active.
Http://www.livescience.com/health/090224-music-memory.html
Music & lyrics are handled separately
http://www.newscientist.com/article/dn18626-music-and-lyrics-how-the-brain-splits-songs.html

People with dyscalculia have a dysfunctional ability to conceptualize numbers just as dyslexics have difficulties with words. Pet & MRI scans show a weak network in the parietal and prefrontal cortices “including the intraparietal sulcus, and the middle and inferior frontal gyrus of both hemispheres. ” indicating this is a critical region for arithmetic calculations
http://www.behavioralandbrainfunctions.com/content/2/1/31

Reading first uses the the left occipital temporal region at the back of the brain to recognize letters then continues through other regions until meaning is processed.
Http://www.healthyplace.com/adhd/add-focus/10-years-of-brain-imaging-research-shows-the-brain-reads-sound-by-sound/menu-id-1580/

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Neuronal Circuits In Autism Can Be Reversed

Editor’s Choice
Main Category: Autism
Article Date: 17 Sep 2012 – 0:00 PDT Current ratings for:
Neuronal Circuits In Autism Can Be Reversed
4 stars3 and a half stars
People with autism suffer from a pervasive developmental disorder of the brain that becomes evident in early childhood.

A specific dysfunction in neuronal circuits has been identified, by Professors Peter Scheiffele and Kaspar Vogt at the Biozentrum of the University of Basel, that results from autism.

The researchers also discovered a way to reverse these neuronal changes. They believe that their findings, published in the journal Science, will have a great effect in drug development for treating autism.

Current estimates have revealed that about 1% of all kids develop an autistic spectrum disorder.

Autism is a hereditary developmental disorder of the brain, where people may experience fixed behavioral traits, disabled social functioning,and restricted speech development.

There are several mutations in over 300 genes identified as a central risk factor for the development of autism. One example is the gene neuroligin-3, which has a role in the formation of synapses- a structure that permits a neuron to pass an electrical or chemical signal to another cell.

Animal studies can be conducted to identify the effects of neuroligin-3 loss. For example, behavioral patterns that reflect important characteristics observed in autism were recognized in mice who did not have the gene for neuroligin-3.

Roche and a team of researchers from the Biozentrum at the University of Basel have detected a fault in the way signals are transmitted through the synapses that change the plasticity and function of the neuronal circuits.

These negative outcomes are associated with an increased output of a particular neuronal glutamate receptor- in charge of regulating the signal transmission between neurons. The brain’s function and development is disrupted over time by an excess of these receptors, which inhibits the adaptation of the synaptic signal transmission during the learning process.

Most importantly, the scientists have discovered that the impaired development of the neuronal circuit in the brain can be reversed.

When the production of neuroligin-3 in the mice was reactivated, the nerve cells reduced the production of the glutamate receptors to a normal level and the structural defects in the brain typical for autism were gone. Consequently, these glutamate receptors could be targeted in the development of drugs that could stop autism from developing or even reverse it.

At present, there is no cure for autism, but the symptoms can be reduced by engaging in behavioral therapy and other treatment.

Fortunately, a new way of treating the disorder has been uncovered through these findings.

In a particular European Union supported project, EU-AIMS, and the research groups from the Biozentrum are working with Roche to figure out how to use glutamate receptor antagonists for the treatment of autism. Researchers hope that in the near future, both adults and children with autism can be successfully treated.

Written by Sarah Glynn
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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posted by Doc Rick on 15 Sep 2012 at 11:12 pm

This article states that “Autism is a hereditary developmental disorder of the brain”. The fact that 1 in 88 kids are now being born with autism (CDC 2012) indicates something deeper than heredity is going on. Autism has spiked in the past 20 years–and men are 4 times as likely to cause autism (Nature 2012). The evidence points to accidental, self-imposed reproductive cell damage by men via RF Energy causing up to 60% of autism. We have the easiest-to-solve public health crisis of our time…and we’re not solving it.

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‘Neuronal Circuits In Autism Can Be Reversed’

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Nerve Stimulation May Be Able To Treat Autism, Stroke, Tinnitus And More

Editor’s Choice
Main Category: Stroke
Also Included In: Autism;  Epilepsy
Article Date: 25 Jul 2012 – 1:00 PDT Current ratings for:
Nerve Stimulation May Be Able To Treat Autism, Stroke, Tinnitus And More
4 and a half stars4 stars
Researchers from UT Dallas explained how specific experiences, like sounds or movements, paired with nerve stimulation can reorganize the brain. This new technology could be the beginning of new treatments for tinnitus, autism, stroke, and other disorders.

The speed, at which the brain works in laboratory animals, could be altered by pairing stimulation of the vagus nerve with fast or slow sounds, according to UT Dallas neuroscientists in a related paper.

Dr. Robert Rennaker and Dr. Michael Kilgard led a group of researchers to examine if neural activity within the laboratory rats’ primary motor cortex would change if it were repeatedly paired with vagus nerve stimulation with a specific movement. They used two groups of rats, pairing the vagus nerve stimulation with movements of the forelimb. The team published their findings in Cerebral Cortex.

The team analyzed the brain activity in response to the stimulation after 5 days of stimulation and movement pairing. They found that the rats that received the stimulation and the training displayed large changes in the organization of the brain’s movement control system. Those that received identical motor training without stimulation pairing did not experience any brain changes, or plasticity.

Attempting to regain motor skills, people who suffer brain trauma or strokes may undergo rehabilitation that involves repeated movement of the affected limb. Experts believe that frequent use of the affected limb leads to reorganization of the brain vital to recovery.

This new research implies that pairing standard therapy with vagus nerve stimulation could result in a faster and more extensive reorganization of the brain. According to Rennaker, associate professor in The University of Texas at Dallas’ School of Behavioral and Brain Sciences, this finding offers the potential to improve and speed up the recovery of a stroke victim.

He said:

“Our goal is to use the brain’s natural neuromodulatory systems to enhance treatments for neurological conditions ranging from chronic pain to motor disorders. Future studies will investigate its effectiveness in treating cognitive impairments.”

Vagus nerve stimulation is known to have an outstanding safety record in epilepsy patients. Knowing this, the technique can provide a new method to treat brain conditions in which the timing of brain responses is abnormal, such as dyslexia and schizophrenia.

Kilgard led another team that paired vagus nerve stimulation with audio tones of speeds at different variations in order to alter the rate of activity within the rats’ brains. Their research, published in the journal Experimental Neurology, showed that this technique induced neural plasticity within the auditory cortex (controls hearing).

MicroTransponder, a biotechnology firm associated with the University, developed a device that the UT Dallas research team is currently working with. MicroTransponder has been testing people in Europe with a vagus nerve stimulation therapy. They hope to eliminate, or reduce, the symptoms of tinnitus, the incapacitated disorder that is often described as “ringing in the ears.”

Kilgard explained:

“Understanding how brain networks self-organize themselves is vitally important to developing new ways to rehabilitate patients diagnosed with autism, dyslexia, stroke, schizophrenia, and Alzheimer’s disease.”

If further research is done that confirms the UT Dallas findings, patients could be treated better with more efficient therapies that are less invasive while avoiding long-term use of drugs.

Written by Sarah Glynn
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our stroke section for the latest news on this subject. Repeatedly Pairing Vagus Nerve Stimulation with a Movement Reorganizes Primary Motor Cortex
Benjamin A. Porter, Navid Khodaparast, Tabbassum Fayyaz, Ryan J. Cheung, Syed S. Ahmed, William A. Vrana, Robert L. Rennaker II and Michael P. Kilgard
Cerebral Cortex doi: 10.1093/cercor/bhr316 Please use one of the following formats to cite this article in your essay, paper or report:

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‘Nerve Stimulation May Be Able To Treat Autism, Stroke, Tinnitus And More’

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Stroke, Tinnitus, Autism And Other Disorders May In Future Be Treated With Nerve Stimulation

Main Category: Stroke
Also Included In: Autism;  Neurology / Neuroscience;  Ear, Nose and Throat
Article Date: 23 Jul 2012 – 0:00 PDT Current ratings for:
Stroke, Tinnitus, Autism And Other Disorders May In Future Be Treated With Nerve Stimulation
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UT Dallas researchers recently demonstrated how nerve stimulation paired with specific experiences, such as movements or sounds, can reorganize the brain. This technology could lead to new treatments for stroke, tinnitus, autism and other disorders.

In a related paper, UT Dallas neuroscientists showed that they could alter the speed at which the brain works in laboratory animals by pairing stimulation of the vagus nerve with fast or slow sounds.

A team led by Dr. Robert Rennaker and Dr. Michael Kilgard looked at whether repeatedly pairing vagus nerve stimulation with a specific movement would change neural activity within the laboratory rats’ primary motor cortex. To test the hypothesis, they paired the vagus nerve stimulation with movements of the forelimb in two groups of rats. The results were published in a recent issue of Cerebral Cortex.

After five days of stimulation and movement pairing, the researchers examined the brain activity in response to the stimulation. The rats who received the training along with the stimulation displayed large changes in the organization of the brain’s movement control system. The animals receiving identical motor training without stimulation pairing did not exhibit any brain changes, or plasticity.

People who suffer strokes or brain trauma often undergo rehabilitation that includes repeated movement of the affected limb in an effort to regain motor skills. It is believed that repeated use of the affected limb causes reorganization of the brain essential to recovery. The recent study suggests that pairing vagus nerve stimulation with standard therapy may result in more rapid and extensive reorganization of the brain, offering the potential for speeding and improving recovery following stroke, said Rennaker, associate professor in The University of Texas at Dallas’ School of Behavioral and Brain Sciences.

“Our goal is to use the brain’s natural neuromodulatory systems to enhance the effectiveness of standard therapies,” Rennaker said. “Our studies in sensory and motor cortex suggest that the technique has the potential to enhance treatments for neurological conditions ranging from chronic pain to motor disorders. Future studies will investigate its effectiveness in treating cognitive impairments.”

Since vagus nerve stimulation has an excellent safety record in human patients with epilepsy, the technique provides a new method to treat brain conditions in which the timing of brain responses is abnormal, including dyslexia and schizophrenia.

In another paper in the journal Experimental Neurology, Kilgard led a team that paired vagus nerve stimulation with audio tones of varying speeds to alter the rate of activity within the rats’ brains. The team reported that this technique induced neural plasticity within the auditory cortex, which controls hearing.

The UT Dallas researchers are working with a device developed by MicroTransponder, a biotechnology firm affiliated with the University. MicroTransponder currently is testing a vagus nerve stimulation therapy on human patients in Europe in hopes of reducing or eliminating the symptoms of tinnitus, the debilitating disorder often described as “ringing in the ears.”

“Understanding how brain networks self-organize themselves is vitally important to developing new ways to rehabilitate patients diagnosed with autism, dyslexia, stroke, schizophrenia and Alzheimer’s disease,” said Kilgard, a professor of neuroscience.

Treatment of neurological disease is currently limited to pharmacological, surgical or behavioral interventions. But this recent research indicates it may be possible to effectively manipulate the plasticity of the human brain for a variety of purposes. Patients then could benefit from brain activity intentionally directed toward rebuilding lost skills.

If subsequent studies confirm the UT Dallas findings, human patients may have access to more efficient therapies that are minimally invasive and avoid long-term use of drugs.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our stroke section for the latest news on this subject. Please use one of the following formats to cite this article in your essay, paper or report:

MLA

University of Texas at Dallas. “Stroke, Tinnitus, Autism And Other Disorders May In Future Be Treated With Nerve Stimulation.” Medical News Today. MediLexicon, Intl., 23 Jul. 2012. Web.
25 Jul. 2012. APA

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posted by ZAFAR AHMED on 23 Jul 2012 at 11:45 am

This news is highly encouraging!!I believe human trials of Microtransponders device for tinnitus are already being carried out. What stage are these trials and how long before the device is available for general use?

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Autism: Its Causes, Diagnosis and Treatment

AUTISM is a puzzling phenomenon that is seen in people of otherwise normal-sometimes above normal-intelligence. However, it is often associated with other problems, and can also appear in mild and severe forms. This variability has led many people to think of it as a spectrum of symptoms rather than a single, clear-cut syndrome and that variability makes it hard to work out what causes it. Researchers say that individuals with Autism Spectrum Disorders are either disinterested in social interactions or find them unpleasant. Sadly, persons with autism spectrum disorders are often painfully aware of their limited sociability, which can lead to profound feelings of sadness and frustration.

CAUSES: Several causes have been attributed to its presence:

(1) A defective SHANK3 gene, which is a human gene on chromosome 22.This gene is a member of the Shank gene family. Shank proteins are present in the brain nerve cells and connect impulses from one nerve cell to the other. Shank proteins also play a role in synapse formation i.e.the points of contact between nerve cells. Researchers from Mount Sinai School of Medicine have found that when one copy of the SHANK3 gene in mice is missing, nerve cells do not effectively communicate and do not show cellular properties associated with normal learning.

(2) They also found altered functional and structural plasticity in nerve cells (which is a cellular measure of the flexibility that occurs during learning) and in the synapses.

(3) So, while there is evidence of genetic influence, but no clear pattern of inheritance, one suggestion that does pop up from time to time is that the process which leads to autism involves faulty mitochondria. The mitochondria are a cell’s power packs. They disassemble sugar molecules and turn the energy thus liberated into a form that biochemical machinery can use. Mitochondrial faults could be caused by broken genes, by environmental effects, or by a combination of the two. If faulty mitochondria do turn out to be a cause of autism, even if not in all cases, that question will have to be investigated. Nerve cells have a huge demand for energy, so a failure of the mitochondria would certainly affect them. The question is, could it cause autism?

Mitochondria from children with autism consumed far less oxygen than those from the control group: Dr Giulivi of the University of California conducted a study on 10 autistic children versus a control group of 10 normal children. She found that mitochondria from children with autism consumed far less oxygen than those from the control group. That is a sign of lower activity. One important set of enzymes-NADH oxidases-used, on average, only a third as much oxygen in autistic children as they did in non-autists, and eight of the autistic children had significantly lower NADH-oxidase activity than is normal.

The mitochondria of the autistic children also leaked damaging oxygen-rich chemicals such as hydrogen peroxide. These are a normal by-product of mitochondrial activity, but are usually mopped up by special enzymes before they can escape and cause harm-for instance, by damaging a cell’s DNA. The level of hydrogen peroxide in the cells of autistic children was twice that found in non-autists. Such high levels suggest the brains of autistic children are exposed to a lot of oxidative stress, something that would probably cause cumulative damage.

DIAGNOSIS: With a new scanning technique via MRI, means an accurate diagnosis of the condition can be made in only 10 minutes. Researchers at Harvard University have made a vital breakthrough in the early diagnosis of autism which shows how the different parts of the brain interact. Autism sufferers have weaker brain connections. The scan shows how well water molecules move along the “wiring”, which links different parts of the brain. From the images, doctors will be able to measure the interaction within the areas of the brain and thus make a diagnosis.

TREATMENT:

(1) Scientists have found that some symptoms of autism can be alleviated by a nasal spray containing oxytocin, the “bonding” hormone. People with autism who inhaled the spray altered their behavior temporarily, becoming more sociable and trusting. “Under oxytocin, patients with high-functioning autism respond more strongly to others and exhibit more appropriate social behavior,” wrote Elissar Andari, of the Institut des Sciences Cognitives, a French government center for neuroscience research, in a summary of a recent conference presentation.

(2) The drug baclofen, which is, in various for has in fact been shown to affect oxytocin. “We published a paper last year showing that baclofen strongly activated oxytocin in the rat brain,” says Iain McGregor at the University of Sydney, Australia

(3) Researchers at the Eastern Virginia Medical School are testing an antibiotic, D-Cycloserine, suggesting it can alter the function of certain receptors in the brain known to affect sociability and help the animals be more at ease around others. EVMS’ laboratory studies on mice have led investigators to hypothesize that D-Cycloserine could ease the impaired sociability of people with autism, such as avoiding eye contact and personal interaction. Those traits can severely limit the possibility of employment and independent living.

(4) Sensory Integration Therapy: Sensory Integration is the process through which the brain organizes and interprets external stimuli such as movement, touch, smell, sight and sound. Autistic children often exhibit symptoms of Sensory Integration Dysfunction (SID) making it difficult for them to process information brought in through the senses. The goal of Sensory Integration Therapy is to facilitate the development of the nervous system’s ability to process sensory input in a more typical way. Through integration the brain pulls together sensory messages and forms coherent information upon which to act. SIT uses neurosensory and neuromotor exercises to improve the brain’s ability to repair itself. When successful, it can improve attention, concentration, listening, comprehension, balance, coordination and impulsivity control in some children.

(5) Speech Therapy: The communications problems of autistic children vary to some degree and may depend on the intellectual and social development of the individual. Some may be completely unable to speak whereas others have well-developed vocabularies and can speak at length on topics that interest them. Any attempt at therapy must begin with an individual assessment of the child’s language abilities by a trained speech and language pathologist.

(6) Occupational Therapy: Occupational Therapy can benefit a person with autism by attempting to improve the quality of life for the individual. The aim is to maintain, improve, or introduce skills that allow an individual to participate as independently as possible in meaningful life activities. Coping skills, fine motor skills, play skills, self help skills, and socialization are all targeted areas to be addressed.

(7) Healing Dynamics: Craniosacral therapy has proven effective in the treatment of Autism. Children with autism feel virtually trapped within themselves. Typically, autistic children have a very tight cranium with no “give”. They often seem to have very severely compressed temporal bones bilaterally and virtually locked occipital sutures. Treatment aims at releasing these sutures and setting free the bones of the cranium. Other treatment methods incorporated in a session include: neurodevelopmental therapy and visceral manipulation.

More information is available at my website: http://www.myhealingdynamics.com

Caroline Konnoth is a Physical Therapist and Owner of Healing Dynamics Corp. Caroline offers a combination of craniosacral,visceral manipulation and lymph drainage therapies and specializes in pediatrics.
Healing Dynamics is a holistic integrative approach, that is a synthesis of several anatomically directed forms of energy healing techniques, resulting in complete physical and emotional balance and harmony. More information is available at: http://myhealingdynamics.com

Article Source: http://EzineArticles.com/?expert=Caroline_Konnoth
http://EzineArticles.com/?Autism:-Its-Causes,-Diagnosis-and-Treatment&id=5624005

Tagged as: Autism Causes, Autism Diagnosis, Autism Treatment

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A Mechanism To Improve Learning And Memory

Main Category: Psychology / Psychiatry
Also Included In: Alzheimer’s / Dementia;  Autism
Article Date: 22 Feb 2012 – 1:00 PST

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There are a number of drugs and experimental conditions that can block cognitive function and impair learning and memory. However, scientists have recently shown that some drugs can actually improve cognitive function, which may have implications for our understanding of cognitive disorders such as Alzheimer’s disease. The new research is reported 21 February in the open-access journal PLoS Biology. The study, led by Drs. Jose A. Esteban, Shira Knafo and Cesar Venero, is the result of collaboration between researchers from The Centro de Biología Molecular Severo Ochoa and UNED (Spain), the Brain Mind Institute (EPFL, Switzerland) and the Department of Neuroscience and Pharmacology (Faculty of Health Sciences, Denmark).

The human brain contains trillions of neuronal connections, called synapses, whose pattern of activity controls all our cognitive functions. These synaptic connections are dynamic and constantly changing in their strength and properties. This process, known as synaptic plasticity, has been proposed as the cellular basis for learning and memory. Indeed, alterations in synaptic plasticity mechanisms are thought to be responsible for multiple cognitive deficits, such as autism, Alzheimer’s disease and several forms of mental retardation.

The study by Knafo et al. provides new information on the molecular mechanisms of synaptic plasticity, and how this process may be manipulated to improve cognitive performance. They find that synapses can be made more plastic by using a small protein fragment (peptide) derived from a neuronal protein involved in cell-to-cell communication. This peptide (called FGL) initiates a cascade of events inside the neuron that results in the facilitation of synaptic plasticity. Specifically, the authors found that FGL triggers the insertion of new neurotransmitter receptors into synapses in a region of the brain called the hippocampus, which is known to be involved in multiple forms of learning and memory. Importantly, when this peptide was administered to rats, their ability to learn and retain spatial information was enhanced.

Dr. Esteban remarks: “We have known for three decades that synaptic connections are not fixed from birth, but they respond to neuronal activity modifying their strength. Thus, outside stimuli will lead to the potentiation of some synapses and the weakening of others. It is precisely this code of ups and downs what allows the brain to store information and form memories during learning”.

Within this framework, these new findings demonstrate that synaptic plasticity mechanisms can be manipulated pharmacologically in adult animals, with the aim of enhancing cognitive ability. Dr. Knafo adds: “These are basic studies on the molecular and cellular processes that control our cognitive function. Nevertheless, they shed light into potential therapeutic avenues for mental disorders where these mechanisms go awry”.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our psychology / psychiatry section for the latest news on this subject. Funding: This work was supported by grants from the Spanish Ministry of Science and Innovation (SAF-2008-04616, SAF-2009-05558-E, CSD-2010-00045, and SAF-2011-24730 to J.A.E; SAF2010-15676 to S.K.; SAF-2009-09129 to C.V.; PI-08/1067 to J.M.S.; SAF-2009-09394 to J.D.F.). In addition, the laboratory of J.A.E. is funded from Fundación Ramón Areces and Institut de France-NRJ; the laboratory of J.D.F. from Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED, CB06/05/0066) and Fundación CIEN; the laboratory of C.S. from the EU (FP7-HEALTH-F2M-2008-201600, MemStick) and the Swiss National Science Foundation (310000-120791). S.K. is the recipient of a “Ramón y Cajal” contract from the Spanish Ministry of Science and Innovation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: I have read the journal’s policy and have the following conflicts: E. Bock and V. Berezin are shareholders of ENKAM Pharmaceuticals A/S, which owns the FGL peptide (less than 0.01% shares each). Nevertheless, this does not alter our adherence to all the PLoS Biology policies on sharing data and materials.
Citation: Knafo S, Venero C, Sa´nchez-Puelles C, Pereda-Pere´z I, Franco A, et al. (2012) Facilitation of AMPA Receptor Synaptic Delivery as a Molecular Mechanism for Cognitive Enhancement. PLoS Biol 10(2): e1001262. doi:10.1371/journal.pbio.1001262
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‘A Mechanism To Improve Learning And Memory’

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