Our speakers for this event will include Eric Hollander MD, Stephen Shore EdD and Michele Robins PhD. Dr. Hollander is the Director of Spectrum Neuroscience and Treatment Institute; a Clinical Professor of Psychiatry and Behavioral Sciences at Albert Einstein College of Medicine and the Director of Autism and Obsessive Compulsive Spectrum Program at Montefiore Medical Center. He is a renowned psychiatrist recognized for his achievements both clinically and in research. Since 2002, Dr. Hollander has been voted into the book “America’s Top Doctors.” Dr. Shore is a special education professor at Adelphi University where his research focuses on matching best practice needs of people with autism. In addition to working with children and talking about life on the autism spectrum, Stephen presents and consults internationally on adult issues pertinent to education, relationships, employment, advocacy, and disclosure as discussed in his books Beyond the Wall: Personal Experiences with Autism and Asperger Syndrome; Ask and Tell: Self-advocacy and Disclosure for People on the Autism Spectrum, and the critically acclaimed Understanding Autism for Dummies. He is the President emeritus of the Asperger’s Association of New England and former board member of the Autism Society.

Dr. Robins is a licensed and school certified psychologist and a clinical/developmental neuropsychologist with expertise in the area of assessment of children, adolescents and adults with learning and emotional problems including ASD. As a past clinical associate at the University of Pennsylvania Medical School, Department of Psychiatry, Dr. Robins consults and lectures widely on the treatment of disorders throughout the lifespan. Dr. Robins uniquely integrates cognitive behavior therapy, family therapy and school consultation to create individualized treatment for individuals with ASD.

Where: Spectrum Neuroscience and Treatment Institute 901 Fifth Avenue NY, NY 10021

When: Wednesday April 24th, 2013; 12:00-2:00 pm

Cost: $100 per person

RSVP to: sw@askstefanie.com

*Please reserve your spot by April 22nd. Space is limited to 15 people.

60 Minutes – Apps for Autism: Communicating on the iPad

A recent 60 Minutes segment titled “Apps for Autism: Communicating on the iPad” discussed how educators and parents are discovering the possible benefits of using an iPad as a form of communication with severely autistic people.  As many as thirty percent of people with autism are unable to speak, and apps such as Proloquo2Go and AutismXpress have made it possible for these individuals to communicate. Proloquo2Go was released for the iPhone in 2009 and was the first augmented (or alternative) communication app, but about 142 apps have been released this year.  In addition, apps have been developed for the Android system. A lot of the apps are based on the Picture Exchange Communication System.

Educators and parents have been amazed by the results.  For example, prior to using an iPad,  28-year old Joshua Hood mostly communicated with family via a form of charades or using a laminated sheet of letters, but after using an iPad, he is capable of communicating much more quickly and can order food at a local diner.  In addition educators at the Beverley School in Toronto, Canada have seen incredible benefits from the use of iPads in the classrooms. The ability to communicate has made it much easier for educators and parents to understand the desires and wishes of the children (e.g., it was discovered that one 10 year-old student at the Beverley School that was believed to have the IQ of a toddler actually has an extensive vocabulary and is a fan of opera and classical music).  The educators and parents believe that the children prefer computers to humans because computers are predictable.

Dr. Walter Schneider from the University of Pittsburgh is currently conducting research to determine if disruptions in the brain’s connective circuits are responsible for the language problems for people with autism.  His first subject for testing was Temple Grandin, the renowned professor and doctor of animal science.  Dr. Schneider scanned Ms. Grandin’s brain and used high definition fiber tracking (an MRI-based test that is also being used to study traumatic brain injuries) to compare her brain with the brain of someone without autism.  The scans show that the wiring in Ms. Grandin’s brain is much more disorganized than the wiring in the brain of the person without autism. Dr. Schneider will need to test more subjects before making any definitive scientific conclusions.

Sources:
http://www.cbsnews.com/8301-18560_162-57460553/apps-for-autism-communicating-on-the-ipad/
http://www.iautism.info/en/2011/03/25/list-of-apps-for-android/#/en/2010/09/20/application-list/
http://www.assistiveware.com/product/proloquo2go
http://autismxpress.com/
http://www.cnn.com/2012/05/14/tech/gaming-gadgets/ipad-autism/index.html
http://www.iautism.info/en/2011/03/25/list-of-apps-for-android/
http://www.pecsusa.com/pecs.php
http://schools.tdsb.on.ca/beverley/
http://schneiderlab.lrdc.pitt.edu/
http://www.cbsnews.com/8301-504803_162-20123944-10391709/temple-grandin-understanding-autism/
http://www.cbsnews.com/video/watch/?id=7385698n
http://www.huffingtonpost.com/2012/03/02/traumatic-brain-injury-high-definition-fiber-tracking_n_1316156.html

The articles and research are mounting with regards to Oxytocin’s possible role in assisting people with autism. Dr. Eric Hollander, Director of the Autism and Obsessive Compulsive Spectrum Program at Albert Einstein College of Medicine/Montefiore Medical Center and Chairman of the ICare4Autism Advisory Council will speak at the ICare4Autism International Autism Conference in August and has been at the forefront of this research since his first publication on the administration of oxytocin to patients with autism in 2003. Oxytocin has a long established role in milk ejection and uterine contraction during labor.  Recent research suggests that oxytocin and the closely related peptide vasopressin play an important role in the development of trust, empathy, social bonding, social affiliation, social threat, perseverative behaviors and overall social behavior and the salience or importance of social signals.

Early observations stem from work in voles, those little furry creatures (they are mouselike rodents related to lemmings). The researchers found two types of voles. Those that were asocial and those that were very social with strong affiliation bonds. The social voles had more oxytocin and vasopressin receptors in their brains than the a social voles. The original studies done by Hollander’s team on the effects of oxytocin infusion in adults with autism showed that oxytocin reduced perseverative behaviors (Neuropsychopharmacology, 2003), improved the retention of social cognition memories (Biological Psychiatry, 2007).  His team’s recent work with intranasal oxytocin has demonstrated effects on social cognition (i.e. recognizing emotions, enhancing empathy; decreasing social stress) and on repetitive behaviors in patients with autism, borderline personality disorder, and healthy adults with social deficits. Work also examines the effect of oxytocin on brain circuitry and gene expression.  Oxytocin stimulates receptors in the regions of the brains that involve social memory and social affiliation, like the amygdala and the thalamus. Further tests on mice and humans using oxytocin and vasopressin show that gene variations may affect response of these hormones on social memory and social cognition.

To quote Dr. Hollander in 2010, “The studies were in both healthy adults and adults with autism. We gave oxytocin via a nasal delivery and by intravenous route. It improved strong trust bonds. It improved emotions that could be read in the eyes. In a study of young adults (above 18 years of age) on the spectrum, Oxytocin therapy lessened the stimming and reduced repetitive behavior. Delivered intravenously and intranasally, it improved social cognition, and improvements were preserved for a two-week period on a single dose.”  This work with oxytocin has been replicated by researchers in Australia (Adam Guastella, Biological Psychiatry 2010) in children with autism where it improved the recognition of emotions and in France (Andari et al, PNAS, 2010) in adults with autism where it improved eye gaze and the choice of appropriate social interaction partners.

International Autism Experts to Gather in Jerusalem: Experts are planning to convene in Jerusalem from around the world in August to learn the latest about Autism Spectrum Disorder (ASD).

Experts are planning to convene in Jerusalem from around the world this August on the issue of Autism Spectrum Disorder (ASD). Thousands of researchers, educators and policy experts will join families affected by the condition at Icare4Autism’s 2012 International Autism Conference, set for August 1-2.

The gathering is aimed at sharing current research into the causes and treatment of ASD, a group of conditions that include Autism, Asperger’s Syndrome (AS) and Pervasive Developmental Disorder (PDD). Hebrew University, the Weitzmann Institute, Tel Aviv University, Haifa University and Bar Ilan University are all partnering with the organization to sponsor the Jerusalem conference.

The conference will focus primarily on the latest developments in biomedical research and practice, education and behavioral research and practice, and ASD policy and awareness.

There will be a special exhibition of innovative assistive technologies for those with autism at the conference, as well as professional workshops led by lecturers from the Hebrew University of Jerusalem.

“We have entered a new era of autism research and advocacy,” said Dr. Joshua Weinstein, CEO and founder of Icare4Autism. “On one hand, we have seen an unprecedented uptick in autism, while at the same time there have been incredible advances made in research and early diagnosis, and more effective intervention.

“It’s a critical period in which the world is beginning to understand – and treat – autism in a more urgent, effective way.”

The conference will be held under the auspices of Jerusalem Mayor Nir Barkat, and headlined by Dame Stephanie Shirley, the first UK Ambassador for Philanthropy, who also heads the Shirley Foundation.

“Research aimed at improving early detection of autism has largely focused on measurement of social and communication development,” said Dr. Rebecca Landa, study author and director of the Center for Autism and Related Disorders at Kennedy Krieger Institute. “However, disruption in early motor development may also provide important clues about developmental disorders such as autism.”

On May 17 in Toronto, Dr. Landa will present this and other new research on motor delay and how it impacts development of language and social skills. The spring International Meeting for Autism Research is an annual scientific meeting providing international researchers with an opportunity to share their findings on ASD.

Before Dr. Landa’s current study, the head-lag text has not been used to diagnose ASD. Her team assessed infants in a “pull-to-sit” task, a simple measure of postural control in infants. Typically developing infants achieve this type of postural control by four months of age.

Dr. Landa’s team studied two groups of infants. The first group consisted of 40 infants, ages 5.6 to 10 months, considered to be at high genetic risk because a sibling had autism. Dr. Landa and her team examined their ability to maintain head alignment when being carefully, yet firmly, pulled by the arms from lying flat on his/her back to a sitting position. Infants were scored according to whether their head maintained alignment with the spine, or was in front of the spine, during the task. Lack of this head control indicated head lag.

The second group examined six-month-olds at a single point in time for the presence of head lag. Dr. Landa and her team found that 75% (n =15) of high-risk infants exhibited head lag, compared to 33% (n =7) of low-risk infants, further supporting that head lag is more likely in infants at risk of developing ASD. “Our findings show that the evaluation of motor skills should be incorporated with other behavioral assessments to yield insights into the very earliest signs of autism,” said Dr. Landa.

“While previous research shows that motor impairments are linked to social and communication deficits in older children with autism, the field is just starting to examine this in younger children,” said Dr. Landa. “Our initial research suggests that motor delays may have an important impact on child development.”

Building on the head lag research, Dr. Landa’s team conducted a separate longitudinal study with 14-, 24- and 36-month-old children at high and low risk of developing ASD. The study found that motor delay becomes increasingly evident as children with ASD near their third birthday, yet not all children with ASD experience motor delay. Results showed that children with ASD who experience motor delays are more severely impaired by three years of age than children with ASD with no motor delays.

“While more research is needed to examine why not all children with ASD experience motor delay, the results of our studies examining motor development add to the body of research demonstrating that early detection and intervention for infants later diagnosed with autism is possible and remains crucial to minimize delays and improve outcomes,” said Dr. Landa.

To reach Dr. Landa’s team at the Kennedy Krieger Institute follow this LINK.

ICare4Autism Founder and President, Joshua Weinstein with Dr. W. Ted Brown

Fragile X and Autism Expert Speaks on Autism in Jerusalem: The Fragile X Syndrome is the most common inherited cause of intellectual disability. Fragile X has a population incidence of approximately 1 in 4,000 affected (full-mutation) males, 1 in 6,000 affected females, 1 in 700 premutation carrier males and 1 in 260 carrier females. This disorder typically causes moderate to severe intellectual deficiency in affected males, and milder deficiency in affected females.  It is associated with autism or PDD-NOS in about 50% of affected males, and most affected individuals evidence some autistic-like behaviors. 

Fragile X syndrome is considered to be the most common known single gene cause of autism. It is estimated that Fragile X accounts for 2-4% of intellectual deficiency overall, and is second to Down syndrome, which is not inherited, as a genetic cause of intellectual deficiency. The fragile X mutation results in the lack of expression of the Fragile X Protein (FMRP), an mRNA finding protein, which results in overexpression of the glutamate (stimulatory) and under-expression of the GABA (inhibitory) pathways in the brain.

Current experimental treatment trails are being carried out in Fragile X and in autism with glutamate receptor blockers and GABA stimulatory drugs.  The underlying defects in neurochemical pathways in both conditions appear to have much in common, involving the ERK, mTOR and PI3K signaling pathways.

Dr. W. Ted Brown will be speaking at the upcoming ICare4Autism International Conference on Autism, in Israel, about the relationship between Fragile X syndrome and autism.

W. Ted Brown, MD, PhD, is the Director of the New York State Institute for Basic Research (IBR) in Developmental Disabilities, Chair of the IBR Department of Human Genetics and Director of the IBR Jervis Clinic.  He is a fellow of the American College of Medical Genetics and Professor at the State University of New York- Downstate Medical Center in Brooklyn.

In 1991, he was appointed the Director of IBR’s Jervis Clinic and in 2005 became IBR’s Director. He is the author of more than 350 publications.  At IBR, he began research focused on the Fragile X syndrome, which was then newly recognized and is now considered to be the most common inherited cause of intellectual deficiency or mental retardation. At IBR, he established a DNA diagnostic and molecular laboratory. He developed a screening and prenatal testing program for Fragile X.

His work on Fragile X has ranged from clinical studies relating to phenotype, to family inheritance studies, to mouse model development, and to basic molecular research. His current research is focused on autism genetics and the Fragile X syndrome.

Eyal Ben-David and Sagiv Shifman, Hebrew University of Jerusalem

Autism Research Finds Disrupted Genetic Systems in Autism: It is widely understood that different genes interact with environmental factors to influence autism, but new research finds a common ground as the various genes involved in autism appear to influence special processes in the brain.

Autism is influenced by many different genes, and different genes are involved in different individuals, making it hard to find the common genetic ground between patients.

Now, research conducted at the Hebrew University of Jerusalem has shown that the different genes involved in autism tend to be involved in specific processes in the brain. This can explain similarities in the behavioral symptoms of different people with autism, but also the large spectrum of behaviors observed in different individuals with autism.

The Hebrew University research, conducted by Dr. Sagiv Shifman and his doctoral student Eyal Ben-David of the Department of Genetics at the Alexander Silberman Institute of Life Sciences, has potential implications for early diagnosis as well as for treatment of autism in the future.

Dr. Shifman’s areas of interest are the genetics of schizophrenia and autism and genetics of variation in gene expression.  He will be speaking about this research “Shared neuronal pathways affected by common and rare variants in autism spectrum disorders” at ICare4Autism’s upcoming International Autism Conference in Jerusalem.

The mission of the Hebrew University project was to test the contribution of rare genetic mutations, as well as the genetic variations which are common in the population, and to see whether these different types of genetic risk factors are related. Instead of testing individual genes, the researchers chose to study gene collections, in an attempt to understand general pathways involved in autism.

Based on genetic data from thousands of families with autistic children, the researchers studied the contribution of different groups of genes to autism.

To their surprise, they found – when looking at mutations found in autism as well as thousands of common gene variants that are more frequently seen in individuals with autism – that these mutations and variations are located in specific functional groups.

When looking at families with one individual with autism (sporadic cases), and in families where there is more than one affected individual (multiplex cases), the same variants were seen acting in both cases. These groups of genes are highly active in the first year of life, and are involved in processes of learning, memory, and sensory perception.

The Hebrew University scientists believe that their work could pave the way for large-scale genetic scans in the future that could allow for early diagnosis of autism. Further, the results of their study provide a ray of hope that by concentrating on specific gene groups, it will one day be possible to design drugs which could alleviate symptom

Ben-David E, Shifman S (2012) Networks of Neuronal Genes Affected by Common and Rare Variants in Autism Spectrum Disorders. PLoS Genet 8(3):e1002556. doi:10.1371/journal.pgen.1002556

http://medicalxpress.com/news/2012-05-genetic-disrupted-autistic-brain.html

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.

“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.”

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.

“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.”

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 http://www.medicalnewstoday.com/releases/244665.php.

Verret, Laure; Mann, Edward O.; Hang, Giao B.; Barth, Albert M.I.; Cobos, Inma; Ho, Kaitlyn; Devidze, Nino; Masliah, Eliezer; Kreitzer, Anatol C.; Mody, Istvan; Mucke, Lennart; Palop, Jorge J. Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model.  Cell doi:10.1016/j.cell.2012.02.046 (volume 149 issue 3 pp.708 – 721)

Young brains are capable of forming many new synapses, and are consequently better at learning new things. That is why we acquire vital skills – walking, talking, hearing and seeing – early on in life. The adult brain stabilizes the synapses so that we can use what we have learned in childhood for the rest of our lives. 

Earlier research found that approximately one fifth of the synapses in the brain inhibit rather than excite other nerve-cell activity. Neuroscientists have now shown that many of these inhibitory synapses vanish if the adult brain is forced to learn new skills. They came to this conclusion by labeling inhibitory synapses in mouse brains with fluorescent proteins and then tracking them for several weeks using a specialized microscope. They then closed one of the mice’s eyes temporarily to accustom them to seeing through just one eye. After a few days, the area of the brain that processes information from both eyes began to respond more actively to the open eye. At the same time, many of the inhibitory synapses disappeared and were later replaced by new synapses.

Inhibitory synapses are essential for the way networks function in the brain. “Think of the excitatory synapses as a road network, with traffic being guided from A to B, and the inhibitory synapses as the matrix signs that regulate the traffic,” explains research leader Christiaan Levelt. “The inhibitory synapses ensure an efficient flow of traffic in the brain. If they don’t, the system becomes overloaded, for example as in epilepsy; if they constantly indicate a speed of 20 kilometres an hour, then everything will grind to a halt, for example when an anaesthetic is administered. If you can move the signs to different locations, you can bring about major changes in traffic flows without having to entirely reroute the road network.”

Inhibitory synapses play a immensely influential role on learning in the young brain. People who have neurodevelopmental disorders – including autism – may have trouble forming inhibitory synapses. The discovery that the adult brain is still capable of pruning or forming these synapses offers hope that pharmacological or genetic intervention can be used to manage this process. This could lead to important guideposts for treating autism, but also repairing damaged brain tissue.

Daniëlle van Versendaal, Rajeev Rajendran, M. Hadi Saiepour, Jan Klooster, Laura Smit-Rigter, Jean-Pierre Sommeijer, Chris I. De Zeeuw, Sonja B. Hofer, J. Alexander Heimel, Christiaan N. Levelt. Elimination of Inhibitory Synapses Is a Major Component of Adult Ocular Dominance Plasticity. Neuron, 2012; 74 (2): 374 DOI:10.1016/j.neuron.2012.03.015

Royal Netherlands Academy of Arts and Sciences. (2012, April 30). “Learning Mechanism Of The Adult Brain Revealed.” Medical News Today. Retrieved from http://www.medicalnewstoday.com/releases/244690.php.

Attendees at past ICare4Autism International Autism Conference

On August 1-2, 2012, more than 1,500 leaders in autism research, educationand policy from every continent will gather in Jerusalem, Israel, for ICare4Autism‘s 2012 International Conference, “Autism: A Global Perspective“.

Dr.Joshua Weinstein, CEO & Founder indicated that the, “Conference will highlight groundbreaking research into the causes and treatments of Autism Spectrum Disorders, and serve as a catalyst for powerful new collaborations to tackle the global autism crisis”.

Students from around the world are invited to present their autism research at a poster session. One poster will be selected by the review committee to receive a scholarship to attend the Conference.  The scholarship will cover travel, hotel accommodations and conference registration fee. The scholarship winner will also be invited to participate on one of the Conference panels. The Poster Session consists of physical displays (aka posters) of information shown during a 60-90 minute session, with presenters standing by their poster reporting empirical research and pilot projects for future research.  Attendees have the opportunity to speak with the presenters about their work.

Dame Stephanie Shirley, The British Government’s Founding Ambassador for Philanthropy, and Chairman of the Shirley Foundation, will deliver the Keynote Address and The First Lady of Panama Mrs. Marta Linares de Martinelli will be giving opening remarks.

They will be joined by distinguished researchers and practitioners from more than 20 countries who will unveil their latest biomedical discoveries andeducational innovations.

Groundbreaking biomedical research will be presented; notably Henry Markram, Ph.D, the Director of Blue Brain Project, Coordinator of the Human Brain Project and Professor at Swiss Federal Institute for Technology (EPFL) will present, “Prospects of using detailed brain simulations to explore possible causes and treatments of Autism”

Innovativeeducational practices will be featured in presentations by Dr. S. Mariam Aljunied (Senior Autism Specialist, Singapore Ministry of Education); Dr.Carlos MarcinSalazar (Director of the National Autism Clinic of Mexico); and Dr. Pamela Wolfberg (Director, Autism Spectrum Program,UniversityofCalifornia San Francisco). Attendees will tour the campus where ICare4Autism will open the world’s first Global Autism Research andEducationCenterin 2015.

ICare4Autism (InternationalCenterfor Autism Research & Education) is a charitable organization, founded in 2004 to catalyze breakthrough innovations in autism research, diagnosis and treatment.