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Einstein researchers contend that scientific evidence directly points to the locus coeruleus–noradrenergic (LC-NA) system as being involved in autism. “The LC-NA system is the only brain system involved both in producing fever and controlling behavior,” says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.

The locus coeruleus has widespread connections to brain regions that process sensory information.

It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another).

“What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks,” says Dr. Mehler.

Drs. Purpura and Mehler hypothesize that in autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors (chemical substances both within as well as outside the genome that regulate the expression of genes). They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.

Drs. Purpura and Mehler believe that, in autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function.

the future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

“You can’t take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it — that’s folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way.”

This study documented that autistic children experience behavior changes during fever.

Einstein researchers contend that scientific evidence directly points to the locus coeruleus–noradrenergic (LC-NA) system as being involved in autism. "The LC-NA system is the only brain system involved both in producing fever and controlling behavior," says co-author Dominick P. Purpura, M.D., dean emeritus and distinguished professor of neuroscience at Einstein.

The locus coeruleus has widespread connections to brain regions that process sensory information. It secretes most of the brain's noradrenaline, a neurotransmitter that plays a key role in arousal mechanisms, such as the "fight or flight" response. It is also involved in a variety of complex behaviors, such as attentional focusing (the ability to concentrate attention on environmental cues relevant to the task in hand, or to switch attention from one task to another). Poor attentional focusing is a defining characteristic of autism.

"What is unique about the locus coeruleus is that it activates almost all higher-order brain centers that are involved in complex cognitive tasks," says Dr. Mehler.

autism, the LC-NA system is dysregulated by the interplay of environment, genetic, and epigenetic factors

They believe that stress plays a central role in dysregulation of the LC-NA system, especially in the latter stages of prenatal development when the fetal brain is particularly vulnerable.

a higher incidence of autism among children whose mothers had been exposed to hurricanes and tropical storms during pregnancy.

autistic children, fever stimulates the LC-NA system, temporarily restoring its normal regulatory function. "This could not happen if autism was caused by a lesion or some structural abnormality of the brain," says Dr. Purpura.

future of autism treatment probably lies in drugs that selectively target certain types of noradrenergic brain receptors or, more likely, in epigenetic therapies targeting genes of the LC-NA system.

If the locus coeruleus is impaired in autism, it is probably because tens or hundreds, maybe even thousands, of genes are dysregulated in subtle and complex ways," says Dr. Mehler. "The only way you can reverse this process is with epigenetic therapies, which, we are beginning to learn, have the ability to coordinate very large integrated gene networks."

"You can't take a complex neuropsychiatric disease that has escaped our understanding for 50 years and in one fell swoop have a therapy that is going to reverse it — that's folly. On the other hand, we now have clues to the neurobiology, the genetics, and the epigenetics of autism. To move forward, we need to invest more money in basic science to look at the genome and the epigenome in a more focused way."

Our increasing exposure to EDCs lends support to a new hypothesis about the cause of autism, called the "extreme male theory." This theory, proposed by Dr. Simon Baron-Cohen and colleagues, speculates that autism is caused by something changing a fetus' hormonal balance that then leads to over-masculinization of the developing brain. Could that "something" be the slurry of hormone-altering chemicals we're exposed to every day? Are EDCs the reason autism-type disorders are 4-9 times more common in boys? (Vaccine side effects never show such lopsided impact on boys versus girls...a glaring fact that is totally ignored by those promoting the vaccine theory of autism.)

Here is where the very interesting link to EDCs comes into play: EDCs often act as weak estrogens and estrogen feminizines the body, but in a fetus' developing brain estrogen actually has the opposite effect...it causes masculinization.

The NCS will establish over one hundred study centers across the US to test the blood of 100,000 newborns for scores of synthetic chemicals, including many EDCs. (Workers have already begun going door-to-door enrolling pregnant moms into the program.) For the next 21 years, scientists will carefully follow the children's health, comparing the body burden of chemicals at birth to diseases developed later in life.

Within 3-4 years, we expect to have enough data accumulated to start detecting what chemicals might be linked to autism.

Beside the NCS, I support other new studies to look at: 1) the autism risk in vaccinated vs. unvaccinated kids; 2) the metabolism of vaccine ingredients (like aluminum, added to make shots work better), 3) more accurate determinations of the true incidence of autism.

A groundbreaking study suggests people with autism-spectrum disorders such as Asperger’s do not lack empathy—rather they feel others’ emotions too intensely to cope.

all the success stories related inside the pages of EPSS are accompanied by fortuitous exposure to various forms of structured material, clearly marking out the most promising path for autistic development and growth.

And of course these discussions fly in the face of the current clamor for early intervention in autism, where it would seem the goal is always to yank the autistic child away as early as possible from his or her preferred method of engaging the world, and substitute instead an intense bombardment of socially based indoctrination, hoping to turn the child around while there is still time for the “malleable” brain to be re-molded.

In my opinion, it is no mere coincidence that the very same elements that stand at the core of the Mottron team's affirmative description of autistic perception and cognition are also the very same elements that stand at the core of humanity’s sudden departure off the savannah and leap into the modern world.

Admittedly, a thorough discussion of such a topic would be much too large for inclusion in an academic research paper such as EPSS, but the fact that the Mottron team does not mention, or even hint at, the connection between the features of autistic perception and the features of human cognitive history leave it unclear whether the team has ever considered such a connection.

At this point in time, the Mottron team seems to be the only autism research team heading in a positive and enlightening direction—a direction that is constructive for autistic individuals everywhere—and I look forward to all their future contributions.

In 2006 your lab published a paper in Nature Neuroscience linking a mirror neuron dysfunction to autism. How might reduced mirror neuron activity explain the symptoms of autism?

Reduced mirror neuron activity obviously weakens the ability of these patients to experience immediately and effortlessly what other people are experiencing, thus making social interactions particularly difficult for these patients. Patients with autism have also often motor problems and language problems. It turns out that a deficit in mirror neurons can in principle explain also these other major symptoms. The motor deficits in autism can be easily explained because mirror neurons are just special types of premotor neurons, brain cells essential for planning and selecting actions. It has been also hypothesized that mirror neurons may be important in language evolution and language acquisition.

Thus, a deficit in mirror neurons can in principle account for three major symptoms of autism, the social, motor and language problems.

There is convincing behavioral evidence linking media violence with imitative violence. Mirror neurons provide a plausible neurobiological mechanism that explains why being exposed to media violence leads to imitative violence.

I think there are two key points to keep in mind. The first one is the one we started with: mirror neurons are brain cells specialized for actions. They are obviously critical cells for social interactions but they can’t explain non-social cognition. The second point to keep in mind is that every brain cell and every neural system does not operate in a vacuum. Everything in the brain is interconnected, so that the activity of each cell reflects the dynamic interactions with other brain cells and other neural systems.

In theory, this finding could lead to educational techniques that could help very young children with autism build their social referencing skills. This could be hugely important for children with autism, since their challenges with "reading" social cues create so many problems as they enter school, interact with peers, and begin to navigate social relationships.

An initial retrospective study is comparing two groups of 20 children initially diagnosed with autism who were functioning well after two or more years of treatment, either with a discrete trial training approach or the DIR approach. The study aims to determine if treatment differences lead to subtle differences in outcome, for example, in terms of flexibility, emotional range, creativity and richness of the child's inner life. Investigators are planning to follow this research with a prospective, randomized, more rigorous study of the two approaches.

"In our previous studies we found out that it looks like you can't just deliver a standard treatment to autistic kids, that there's so much variability among the children that what works for one child doesn't work for another child," he says. "Our hypothesis is that...unless you individualize treatment, you're not going to get the best effect."

Researchers at the University of Maryland are testing an intervention to trigger children's "social engagement system," which includes behaviors such as listening, looking, facial expressions and vocalizations that support social interaction, says psychologist Stephen Porges, PhD. The treatment is designed to improve autistic children's ability to interact with others, thereby making them more receptive to traditional therapies.

The intervention is based on the theory that tensing the middle ear muscles enables people to pick out the human voice from lower frequency sounds in the environment, Porges says. Treatment involves exercising middle ear muscles by playing music that has been altered to include only frequencies associated with the human voice, which improves one's ability to listen to human voices. This, in turn, stimulates the entire social engagement system, Porges says. About 80 percent of 50 children with autism or other behavioral problems receiving this treatment via five 45-minute sessions in a double blind, randomized controlled study showed marked improvements in listening, language and other communication skills.

In a report last year in the Journal of Autism and Developmental Disorders (Vol. 28, No. 1, p. 15-23) evaluating an intensive home-based discrete trial training intervention, Stephen Sheinkopf, PhD, of the University of Miami and Bryna Siegel, PhD, of the University of California, San Francisco, noted that children receiving an average of only 21 hours per week of treatment showed gains in IQ comparable to those achieved by children receiving 32 hours per week. The intensity question remains an issue of importance for the autism community. "If we need 40 hours a week, fine," says psychologist Geraldine Dawson, PhD, of the University of Washington. "But if you only need 25, you have to realize that 40 hours is a tremendous burden not only financially, but on families and on the child."