Different genes may cause autism in boys and girls

Like detectives trying to solve a murder case, researchers searching for the biological cause of autism have come up with some surprising suspects.

They've found that different genes may be responsible for causing autism in boys than in girls.

In addition, the researchers also have discovered that other genes may play a role in the early onset form of the developmental disorder and in the recently verified regression, or late onset, type of autism, according to a new study published today in the online edition of the journal Molecular Genetics.

The study also provides new evidence for the idea that multiple genes contribute to autism, said lead author Gerard Schellenberg, a researcher at the Puget Sound Veterans Affairs Medical Center and a research professor of medicine at the University of Washington. The research team was headed by Schellenberg, Ellen Wijsman, a UW research professor of medical genetics and Geraldine Dawson, director of the UW's Autism Center.

"It is highly unlikely that there is only one gene responsible for autism," said Schellenberg. "There may be four to six major genes and 20 to 30 others that might contribute to autism to a lesser degree.

"If an individual only gets three high-risk variants of these genes, it could mean a less-severe form of autism. And because autism is rarer in females, it may take more risk genes for a female to have autism. There also is the possibility that there might be a biological difference in autism for females versus males," he said.

"What is meaningful is that we have found evidence for two genetic subtypes of autism, male versus female and early versus late onset," added Geraldine Dawson, a professor of psychology. "This is a critical piece of information. With Alzheimer's disease research, one big breakthrough was segregating the late and early onset forms of the disease, and this led to important genetic discoveries."

Schellenberg said the study came up with "strong support" for an autism gene on chromosome 7 and "less, but still compelling evidence" for genes on chromosomes 3, 4 and 11. These results confirm some data from previous studies, particularly involving chromosome 7.

The search for autism genes is part of a long-term Autism Center effort to uncover the genetic and neurobiological causes of autism. To find regions of the human genome that contain autism genes, the researchers scanned the DNA of 169 families that had at least two siblings who met the strict criteria for autism. They also scanned the DNA of another 54 families that, in addition to having individuals with strictly defined autism, also included members who had less severe forms of the disorder, such as Asperger syndrome.

"We have been working almost 10 years to get to this point," said Schellenberg. "If we can find and confirm that a particular gene is involved in autism the field will explode. We have to find a gene so that molecular biology can be defined and we can understand what's inside autism. Until that happens, we are dancing on the outside."

Dawson said the researchers are looking for autism susceptibility genes, ones that heighten the risk of an individual getting autism, just as there are genes that raise the chances of getting breast cancer.

"Once we discover these susceptibility genes, we can immediately screen infants to identify those at risk early in life. Early identification can lead to early intervention, which could have a much more dramatic effect.

"Also, when a gene is discovered, you discover the underlying biology of autism at the molecular level. Once you understand the biology you can develop a prevention strategy including medical approaches. Genetic research is a good strategy for eventually designing effective medical treatments for autism," she said.

From University of Washington

Autisme: laissez Freud en dehors de tout ça!

VIRGINIE POYETTON
Le Courrier (Genève)

PRISE EN CHARGE - L'autisme: psychose ou handicap? Des parents demandent que cesse la prise en charge psychanalytique et que des écoles spécialisées soient créées à Genève.

«J'avais vu des émissions à la télévision. Un enfant qui, à 3 ans, range ses livres de manière obsessionnelle, aligne des petits cailloux ou sélectionne ses aliments, ce n'est pas normal. Je suis allée à la guidance infantile. J'ai demandé: ''est-il est autiste?'' On m'a répondu: ''Non. Il a des troubles du comportement.'' C'était vague. Mais, du coup, ça m'a soulagée.» Deux ans plus tard, le fils de Marie-Jeanne Accietto est diagnostiqué «autiste».
Déçue par le peu de soutien qu'elle reçoit des institutions, et insatisfaite des soins prodigués à son fils en centre de jour – elle juge l'approche psychanalytique inadéquate –, elle décide de s'occuper partiellement de l'éducation de son enfant.
Avec quelque vingt-cinq familles, Marie-Jeanne Accietto a créé un groupe de parents d'enfants autistes. Ce dernier demande que l'autisme soit reconnu comme handicap à part entière et revendique une prise en charge spécialisée des enfants autistes (lire ci-contre). Dans un premier temps, pour former des professionnels spécialisés en autisme et établir des diagnostics, il demande la création d'un centre de compétence en autisme. Finalement, la création de trois écoles spécialisées pour autistes devrait permettre d'apporter une prise en charge spécifique. Un projet a été mis sur papier et envoyé au professeur Eliez, directeur du Service médico-pédagogique de Genève (SMP).

«Il est difficile de faire admettre la spécificité de l'autisme»

En premier lieu, les parents regrettent l'absence de choix réel dans l'approche thérapeutique/éducative. «La psychanalyse est la seule approche utilisée par les institutions. C'est un vrai diktat.» Selon cette théorie, le rôle des parents doit être minimal, soutient Mme Accietto. De nombreux pères et mères se sentent désarmés. «La psychologue de référence du centre de jour où mon fils a été placé m'a dit: «Pleurez un bon coup et ça passera! On a l'impression de ne pas être entendus. On nous taxe d'anxieux. On nous renvoie une image très culpabilisante de nous-mêmes.» «C'est vrai qu'il y a un besoin spécifique de prise en charge de type éducatif pour les enfants autistes à Genève», affirme Anne Emery-Torracinta, présidente d'insieme-Genève, (association de parents de personnes mentalement handicapées).
Pour le directeur du SMP, une approche uniquement psychanalytique est insuffisante. «L'autisme a une multitude de causalités. Il n'existe pas de traitement unique. Nous devons travailler sur une approche plus cognitive.» De là, le professeur en vient à la proposition des parents de créer un centre de compétence: «L'idée fait sens. Mais un tel centre implique une régionalisation et donc des inégalités d'accès pour les parents qui voudraient faire diagnostiquer leur enfant. Et le réseau de soins genevois a au contraire cherché à développer un réseau de proximité.» L'idée semble donc enterrée. Pourtant, pour Marie-Jeanne Accietto, la régionalisation n'est pas une entrave à sa réalisation. Elle soutient que les éducateurs spécialisés, s'agissant de l'autisme, manquent de formation. Le nouveau centre de compétence permettrait aux professionnels d'être informés des différentes méthodes et des avancées scientifiques en matière de prise en charge des enfants autistes. «Il pourrait servir de centre de diagnostic et d'évaluation», complète Mme Emery-Torracinta. «Il est difficile de faire admettre la spécificité de l'autisme, confie Mme Accietto. Pour les institutions publiques, parler de spécificité, c'est enfermer l'autiste dans un ghetto.» Pourtant, pour la jeune mère, la reconnaissance du handicap est primordiale pour aider l'enfant. «Est-ce que vous allez au service orthopédique quand vous souffrez d'une tumeur?» L'absence de diagnostic est perturbante pour de nombreux parents. «Laisser les parents dans le vague, les empêche d'agir, de se renseigner, de comprendre. C'est absurde. Nous souhaitons que le diagnostic soit posé avant l'âge de 3 ans. Même s'il y a un doute. Il faut au moins avertir les parents.» Pour le professeur Eliez, cette revendication est plus que légitime. «Dans ce sens, il faut souligner le rôle essentiel joué par les pédiatres de ville.» Il y a trois ans, le professeur organisait une formation sur l'autisme pour les pédiatres, «mais ce sont des démarches qui doivent être répétées en boucle». Et qui visiblement rencontrent encore de fortes résistances.

Globalement, tous s'accordent sur la nécessité de faciliter l'accès aux classes dites normales

Dans un deuxième temps, les parents du groupe demandent la création d'écoles spécialisées en autisme (une pour les 4-12 ans, et deux pour les 12-18 ans) avec une intégration partielle dans des classes dites normales pour les enfants les plus avancés. Aujourd'hui, les enfants sont placés dans des centres de jour avec d'autres enfants handicapés ou dans des institutions privées. Le professeur Eliez est fermement opposé à la création de telles écoles: «Il n'est pas souhaitable de regrouper des enfants autistes. Les enfants, de manière générale, interagissent. Il est très positif pour les autistes d'être en contact avec leurs pairs. Ce serait une ségrégation contre-productive.» Plus nuancée, Mme Emery-Torracinta avoue n'avoir pas été complètement convaincue par ce projet: «Nous souhaitons évidemment un personnel spécialisé, mais pas à tout prix une école spécifique. Enfin, ça se discute. Mais comme cela fait des années que les parents demandent une prise en charge adaptée, il est normal qu'ils en viennent à demander une école.»
Globalement, tous s'accordent sur la nécessité de faciliter l'accès aux classes dites normales. Un projet de loi est en discussion au Grand Conseil et une classe intégrée ouvrira aux Crêts-de-Champel à la rentrée prochaine.

Les autistes males ont moins de neurones dans l’amygdale

Par David Biello, Scientific American

De nombreux garçons et hommes atteints d’autisme souffrent d’une diminution de leurs capacités de communication et sociales réduites. Ils pourraient aussi souffrir d’un manque de neurones dans l’amygdale, selon les découvertes d’une nouvelle étude. David Amaral et Cynthia Mills Schumann de l’université de Californie à Davis, ont étudié le nombre de neurones dans l’amygdale de neuf autistes mâles et de 10 mâles non-autistes dont les âges variaient entre 10 to 44 ans. Comptant péniblement leur nombre sous un microscope, ils ont observé une quantité significativement moindre de neurones (des cellules de signalisation électrique) dans cette zone du cerveau associée à la peur et la mémoire.

"C’est la première preuve quantitative d’un nombre anormal de neurones dans l’amygdale des autistes," note Amaral. "Nous avons pu analyser post-mortem plus du double de cerveaux qu’avant, dont aucun n’avait eu d’attaque ou autres troubles neurologiques, mis à part l’autisme.

Des études précédentes s’étaient appuyées sur des mesures de densité des neurones ainsi que sur le cerveau d’autistes mâles ayant eu des attaques épileptiques--un état que l’ont sait provoquer des défauts de l’amygdale. Amaral et Schumann ont compté des neurones avec une sonde tridimensionnelle à fort grossissement. Ils ont trouvé que bien qu’il n’y ait pas de variation dans le volume de l’amygdale, celle du groupe des autistes mâles avait globalement 1,5 million de neurones en moins que celle de leurs pairs.

D’autres études utilisant l’imagerie cérébrale ont montré que les garçons autistes développent une amygdale adulte vers l’âge de huit ans, alors que les autres garçons l’atteignent à l’adolescence. On ne sait pas encore s’il y a d’autres régions du cerveau des autistes qui pourraient avoir un déficit de neurones. "Il est possible qu’il y ait toujours moins de neurones dans l’amygdale des personnes atteintes d’autisme. Il est aussi possible qu’un processus de dégénérescence se déclenche plus tard dans la vie et conduise à une perte de neurones," dit Schumann. "Des études complémentaires sont nécessaires pour affiner nos découvertes." Celles-ci sont publiées dans un article qui paraît aujourd’hui dans le Journal of Neuroscience.

Un pas de plus dans la recherche sur l’autisme

Laurent Suply (lefigaro.fr)

Les causes de ce trouble psychologique sont encore loin d’être élucidées, mais une étude américaine publié mercredi dans le Journal of Neuroscience démontre que les personnes souffrant d’autisme ont moins de neurones dans une zone du cerveau dont dépend l’expression des émotions et le comportement social.

Dix-neuf cerveaux appartenant à des personnes décédées de 10 et 44 ans, dont neuf souffraient d’autisme, ont été examinés par les chercheurs de l’université américaine de Californie. Grâce à une technique nommée « analyse stéréologique », ces chercheurs ont pu dénombrer les neurones des cerveaux dans une zone appelée « amygdale », pour sa forme d’amande. Résultat: les autistes possèdent un nombre significativement inférieur de neurones dans cette région du cerveau, une conclusion qui vient confirmer le lien pressenti entre cette zone et l’autisme.


Le lien entre l’autisme et l’amygdale était déjà pressenti


L’amygdale est une partie du cerveau qui intervient notamment dans le processus de mémorisation des émotions et dans le développement des comportements sociaux. Elle intervient par exemple dans l’apprentissage de la peur. Elle sert également à décrypter les émotions de nos proches. Une étude précédente a montré que l’amygdale s’active lorsqu’il s’agit de deviner les émotions d’autrui en regardant les expressions de son visage. Chez les sujets autistes, l’activation de cette zone n’a pas lieu dans cette situation.


« Ces découvertes complètent d’autres études qui suggéraient que des anomalies de l’amygdale contribuaient significativement au déficit de fonctions sociales » qui définissent l’autisme, explique Emanuel DiCicco-Bloom, professeur de neurologie pédiatrique à l’Université de médecine du New Jersey. Le résultat de l’étude, publiée par le Journal of Neuroscience est jugé « un peu surprenant » par Cynthia Schumann, un des auteurs de l’étude. Des études d’imagerie magnétique antérieures avaient montré que l’amygdale était sensiblement plus grosse en volume chez les jeunes garçons souffrant d’autisme que les sujets « sains ».


Prochaine étape : observer l’évolution des neurones tout au long de la vie


Grâce à l’étude de l’Université de Californie, le lien semble désormais certain. Mais elle n’assure pas pour autant que la déficience de l’amygdale soit la cause de l’autisme. Plusieurs hypothèses sont envisagées. Le déficit neuronal peut tout d’abord dater de la naissance du sujet, ou au contraire découler d’un processus de dégénérescence causant l’autisme. Autre possibilité, l’atrophie neuronale de l’amygdale est la conséquence de l’autisme : à force de ne pas être « utilisés » par le malade, les neurones chargés des émotions disparaissent. Une telle perte pourrait enfin être causée par le très haut niveau d’anxiété ressenti par les intéressés.


Le lien mystérieux entre l’amygdale et ce trouble du comportement devra donc être exploré plus avant. Pour ce faire, l’une des pistes consiste à développer des techniques permettant de compter les neurones de personnes en vie, afin d’observer l’évolution de leur quantité chez des jeunes sujets autistes. La recherche sur ce trouble psychologique est « un processus à plusieurs étapes », souligne David Amaral, autre membre du groupe d’étude, qui ajoute : « Au moins, nous en avons franchi une de plus ».

Researchers gain insight into why brain areas fail to work together in autism

Researchers have found in two studies that autism may involve a lack of connections and coordination in separate areas of the brain.

In people with autism, the brain areas that perform complex analysis appear less likely to work together during problem solving tasks than in people who do not have the disorder, report researchers working in a network funded by the National Institutes of Health. The researchers found that communications between these higher-order centers in the brains of people with autism appear to be directly related to the thickness of the anatomical connections between them.

In a separate report, the same research team found that, in people with autism, brain areas normally associated with visual tasks also appear to be active during language-related tasks, providing evidence to explain a bias towards visual thinking common in autism.

"These findings provide support to a new theory that views autism as a failure of brain regions to communicate with each other," said Duane Alexander, M.D., Director of NIH's National Institute of Child Health and Human Development. "The findings may one day provide the basis for improved treatments for autism that stimulate communication between brain areas."

The studies and the theory are the work of Marcel Just, Ph.D., D.O. Hebb Professor of Psychology at Carnegie Mellon University in Pittsburgh, Pennsylvania, and Nancy Minshew, M.D., Professor of Psychiatry and Neurology at the University of Pittsburgh School of Medicine and their colleagues. The research was conducted by the Collaborative Program of Excellence in Autism, a research network funded by the NICHD and the National Institute on Deafness and Other Communication Disorders.

People with autism often have difficulty communicating and interacting socially with other people. The saying "unable to see the forest for the trees" describes how people with autism frequently excel at details, yet struggle to comprehend the larger picture. For example, some children with autism may become spelling bee champions, but have difficulty understanding the meaning of a sentence or a story.

An earlier finding by these researchers described how a group of people with autism tended to use parts of the brain typically associated with processing shapes to remember letters of the alphabet. A news release detailing that finding appears at http://www.nichd.nih.gov/new/releases/final_autism.cfm.

Participants with autism in both current studies had normal I.Q. There were no significant differences between the participants with and without autism in age or I.Q.

The first of the two new studies recently was published online in the journal Cerebral Cortex. In that study, the researchers used a brain imaging technique known as functional magnetic resonance imaging, or fMRI, to view the brains of people with autism as well as a comparison group of people who do not have autism. All of the study participants were asked to complete the Tower of London test. The task involves moving three balls into a specified arrangement in an array of three receptacles. The Tower of London is used to gauge the functioning of the prefrontal cortex.

This brain area, located in the front, upper part of the brain, deals with strategic planning and problem-solving. The prefrontal cortex is the executive area of the brain, in which decision making, judgment, and impulse control reside.

A little further back is the parietal cortex, which controls high-level visual thinking and visual imagery, supporting the visual aspects of the problem-solving. Both the prefrontal and parietal cortex play a critical part in performing the Tower of London test.

In the normal participants, the prefrontal cortex and the parietal cortex tended to function in synchrony (increasing and decreasing their activity at the same time) while solving the Tower of London task. This suggests that the two brain areas were working together to solve the problem.

In the participants with autism, however, the two brain areas, prefrontal and parietal, were less likely to function in synchrony while working on the task.

The researchers made another discovery, for the first time finding a relationship between this lower level of synchrony and the properties of some of the neurological "cables" or white matter fiber tracts that connect brain areas.

White matter consists of fibers that, like cabling, connect brain areas. The largest of the white matter tracts is known as the corpus callosum, which allows communication between the two hemispheres (halves) of the brain.

"The size of the corpus callosum was smaller in the group with autism, suggesting that inter-regional brain cabling is disrupted in autism," Dr. Just said.

In essence, the extent to which the two key brain areas (prefrontal and parietal) of the autistic participants worked in synchrony was correlated with the size of the corpus callosum. The smaller the corpus callosum, the less likely the two areas were to function in synchrony. In the normal participants, however, the size of the corpus callosum did not appear to be correlated with the ability of the two areas to work in synchrony.

"This finding provides strong evidence that autism is a disorder involving the biological connections and the coordination of processing between brain areas," Dr. Just said.

He added, however, that the thickness, or extent, of connections between brain areas may not be the basis for the disorder. Although the neurological connections between the prefrontal cortex appear to be reduced in autism, the brains of people with autism have thicker connections between certain brain regions within each hemisphere.

"At this point, we can say that autism appears to be a disorder of abnormal neurological and informational connections of the brain, but we can't yet explain the nature of that abnormality," Dr. Just said.

In the second study, published online in the journal Brain, the researchers examined the extent to which brain areas involved in language interact with brain regions that process images. Dr. Just explained that earlier studies, as well as anecdotal accounts, suggest that people with autism rely more heavily on visual and spatial areas of the brain than do other people.

In this study, the researchers used fMRI to examine brain functioning in participants with autism and in normal participants during a true-false test involving reading sentences with low imagery content and high imagery content. A typical low imagery sentence consisted of constructions like "Addition, subtraction, and multiplication are all math skills." A high imagery sentence, "The number eight when rotated 90 degrees looks like a pair of eyeglasses," would first activate left prefrontal brain areas involved with language, and then would involve parietal areas dealing with vision and imagery as the study participant mentally manipulated the number eight.

As the researchers expected, the visual brain areas of the normal participants were active only when evaluating sentences with imagery content. In contrast, the visual centers in the brains of participants with autism were active when evaluating both high imagery and low imagery sentences.

"The heavy reliance on visualization in people with autism may be an adaptation to compensate for a diminished ability to call on prefrontal regions of the brain," Dr. Just said.

The second study also confirmed the observations in the first study--that the prefrontal and parietal brain regions of the cortex in people with autism were less likely to work in synchrony than were the brains of normal volunteers. The second study also confirmed that the extent to which the two parts of the cortex could work together was correlated with the size of the corpus callosum that connected them. Dr. Just and his colleagues are conducting additional studies to ascertain the nature of the abnormality of the connections in the brains of people with autism.

New Model Of Brain Sheds Light On Triggers Of Autism

Science Daily — Approximately 1.5 million children and adults in the U.S. have autism and it is estimated to be the fastest growing developmental disability with a 10 – 17 percent increase each year. While much is known about the symptoms of autism, the exact cause of the condition is not yet defined.

A new model of the brain developed by Dr. Stephen Grossberg, professor and chairman of the Department of Cognitive and Neural Systems at Boston University, and Dr. Don Seidman, a pediatrician with the DuPage Medical Group in Elmhurst, IL, sheds light on the triggers of behaviors commonly associated with autism. The paper, “Neural Dynamics of Autistic Behaviors: Cognitive, Emotional, and Timing Substrates,” appears in the July issue of the journal Psychological Review, published by the American Psychological Association.

“Autism involves multiple genes and correspondingly, people with autism are known to have multiple cognitive, emotional, and motor symptoms – such as impaired development of speech and difficulty expressing emotions,” said Dr. Grossberg. “The iSTART model describes the various brain mechanisms that underlie autism and how they may give rise to the symptoms of the condition.”

iSTART, which stands for Imbalanced Spectrally Timed Adaptive Resonance Theory, is derived from the earlier START model developed by Grossberg to explain how the brain controls normal behaviors. The new model describes how brain mechanisms that control normal emotional, timing, and motor processes may become imbalanced and lead to symptoms of autism. START and its imbalanced version iSTART are a combination of three models, each one of which tries to explain fundamental issues about human learning and behavior.

The first, called Adaptive Resonance Theory, or ART, proposes how the brain learns to recognize objects and events. Recognition is accomplished through interactions between perceptually-driven inputs and learned expectations. Inputs attempt to match expectations which helps prompt the brain to anticipate input/expectation patterns.

“When a match occurs, the system locks into a resonant state that drives how we learn to recognize things; hence the term adaptive resonance,” explained Grossberg.

The degree of match that is required for resonance to occur is set by a vigilance parameter which controls whether a particular learned representation will be concrete or abstract. Low vigilance allows for learning of broad abstract recognition categories, such as a category that is activated by any face; high vigilance forces the learning of specific concrete categories, such as a category that is activated by a particular view of a familiar friend’s face. iSTART proposes that individuals with autism have their vigilance fixed at such a high setting that their learned representations are very concrete, or hyperspecific.

“Hypervigilance leads to hyperspecific learning which perpetuates a multitude of problems with learning, cognition, and attention,” said Grossberg.

The second model, called the Cognitive-Emotional-Motor, or CogEM, model, extends ART to the learning of cognitive-emotional associations, or associations that link objects and events in the world to feelings and emotions that give these objects and events value. Under normal circumstances, arousal of the circuits in the brain that control emotion are set at an intermediate level. Either under-arousal or over-arousal of these circuits can cause abnormal emotional reactions and problems with cognitive-emotional learning.

“If the emotional center is over-aroused, the threshold to activate a reaction is abnormally low, but the intensity of the emotion is abnormally small,” said Grossberg. “In contrast, if the emotional circuits are under-aroused, the threshold for activating an emotion is abnormally high, but when this threshold is exceeded, the emotional response can be over reactive. The iSTART model proposes that individuals with autism experience under-aroused emotional depression which helps explain symptoms like reduced emotional expression as well as emotional outbursts.”

The third model, called the Spectral Timing model, clarifies how the brain adaptively times responses in order to acquire rewards and other goals. iSTART shows how individuals with autism experience failures of adaptive timing that lead to the premature release of behaviors which are then unrewarded.

“iSTART depicts how autistic symptoms may arise from breakdowns in normal brain processes, notably a combination of under-stimulated emotional depression in the amygdala and related brain regions, learning of hyperspecific recognition categories in the temporal and prefrontal cortices, and breakdowns of adaptively timed attention and motor circuits in the hippocampal system and cerebellum,” said Grossberg. “The model clarifies how malfunctions in these mechanisms can, though a system-wide vicious circle, cause and maintain problems with them all.”

According to the researchers, iSTART is a breakthrough in the understanding of the many factors that contribute to autism and provides a unifying perspective that connects autistic symptoms to brain mechanisms that have no obvious connection to the condition.

"This approach should make it easier for scientists studying normal behavior to connect their work to autism research," said Grossberg. "iSTART opens up a wide range of possible new experiments to evaluate autistic behaviors and further test and develop the model.”

More information about iSTART and its component models can be found at http://www.cns.bu.edu/Profiles/Grossberg.

Note: This story has been adapted from a news release issued by Boston University.

Study clears MMR vaccine of autism link

Pervasive developmental disorders (PDD) like autism and Asperger Syndrome have been on the rise for years. Measles Mumps Rubella (MMR) vaccines and thimerosal–containing vaccines (which are approximately 50 percent ethylmercury) have been suggested as possible causes. A new MUHC study published in the scientific journal Pediatrics tomorrow, assesses the link between childhood immunizations and PDD in 28,000 Quebec children and finally clears MMR vaccines and thimerosal–containing immunizations as risk factors.

"There is no relationship between the level of exposure to MMR vaccines and thimerosal–containing vaccines and rates of autism," says Dr. Eric Fombonne, Director of Pediatric Psychiatry at The Montreal Children's Hospital of the MUHC and lead investigator of the new study. Thimerosal was used to prevent bacterial and fungal contamination in the manufacture of various vaccines until its elimination from vaccine formulas in 1996 in Quebec. "According to our data, the incidence of autism was higher in children who were vaccinated after thimerosal was eliminated from vaccines," says Dr. Fombonne.

"In the past, concern about a potential link between MMR vaccinations and autism led some parents to take the drastic step of refusing to inoculate their children against dangerous childhood diseases like measles," says Dr. Fombonne. "This action resulted in resurgence of the measles, which caused the deaths of several young children in Europe." Dr. Fombonne's study indicates that autism rates continued to increase even with reductions in the use of MMR vaccinations. "We hopes this study will finally put to rest the pervasive belief linking vaccines with developmental diseases like autism," says Dr. Fombonne.

Autism is a neuropsychiatry disorder that impairs a child's ability to communicate and interact with others. The prevalence is about 65 cases per 10,000 people (about 1 child in 155) making autism one of the most common childhood disorders. The Psychiatry Department at The Montreal Children's Hospital sees about 350 new cases of autism each year. However, Dr. Fombonne stresses that there is no demonstrated autism epidemic. He attributes the rise in autism rates to a broader definition of autism and greater awareness of the disorder.

From McGill University