“Having at our fingertips detailed information about when and where specific gene products are expressed in the brain brings new hope for understanding how this process can go awry in schizophrenia, autism and other brain disorders,” said NIMH Director Thomas R. Insel, M.D.

Among key findings in the prefrontal cortex:Individual genetic variations are profoundly linked to expression patterns. The most similarity across individuals is detected early in development and again as we approach the end of life.Different types of related genes are expressed during prenatal development, infancy, and childhood, so that each of these stages shows a relatively distinct transcriptional identity. Three-fourths of genes reverse their direction of expression after birth, with most switching from on to off.Expression of genes involved in cell division declines prenatally and in infancy, while expression of genes important for making synapses, or connections between brain cells, increases. In contrast, genes required for neuronal projections decline after birth – likely as unused connections are pruned.By the time we reach our 50s, overall gene expression begins to increase, mirroring the sharp reversal of fetal expression changes that occur in infancy.Genetic variation in the genome as a whole showed no effect on variation in the transcriptome as a whole, despite how genetically distant individuals might be. Hence, human cortexes have a consistent molecular architecture, despite our diversity.

Among key findings:Over 90 percent of the genes expressed in the brain are differentially regulated across brain regions and/or over developmental time periods. There are also widespread differences across region and time periods in the combination of a gene’s exons that are expressed.Timing and location are far more influential in regulating gene expression than gender, ethnicity or individual variation.Among 29 modules of co-expressed genes identified, each had distinct expression patterns and represented different biological processes. Genetic variation in some of the most well-connected genes in these modules, called hub genes, has previously been linked to mental disorders, including schizophrenia and depression.Telltale similarities in expression profiles with genes previously implicated in schizophrenia and autism are providing leads to discovery of other genes potentially involved in those disorders.Sex differences in the risk for certain mental disorders may be traceable to transcriptional mechanisms. More than three-fourths of 159 genes expressed differentially between the sexes were male-biased, most prenatally. Some genes found to have such sex-biased expression had previously been associated with disorders that affect males more than females, such as schizophrenia, Williams syndrome, and autism.

"With a facilitator guiding her arm, the child who had never been taught to read was suddenly writing poetry and English essays, taking history exams and doing algebra. The middle-schooler who couldn't put on her coat without help was typing about her plans to become a college professor,"

But the technique, in which the aide's hand is supposedly guided by the child to type what she wants to say, has been proved ineffective. It has been shown to rely on the aide's projections rather than to reflect the child's thoughts. Although some autistic children can learn to communicate genuinely via a keyboard with only initial guidance, facilitated communication, in which an aide always does the typing has repeatedly failed to demonstrate that the words are written or thought by the child. For example, when the facilitator is not allowed to hear the questions being asked of the child, the resulting answers are wrong or nonsensical.

When the Wendrow's daughter's aide typed allegations of sexual abuse against the girl's father and brother — and claimed that the child's mother had been ignoring her complaints — a prosecution of the family was set into motion that became nearly unstoppable. The aide refused to believe she was not typing her own ideas, even though the child was clearly not capable of the complex language being attributed to her. Once prosecutors and the aide became convinced of the truth of the allegations, even overwhelming evidence of their falsehood was ignored.

The American Psychiatric Association (APA) is now in the process of developing and finalizing the new Diagnostic and Statistical Manual of Mental Disorders (DSM) Version 5.

autism spectrum disorders as we know them will change radically, and many people who are now considered to be "autistic" may find themselves with a brand new diagnosis.

Unless something changes between now and then, as of 2013, Asperger syndrome will no longer exist as a diagnosis.

The Howard Hughes Medical Institute describes how researchers using "high-throughput gene sequencing technology" were able to identify several de novo or spontaneous gene mutations in 20 children with sporadic autism spectrum disorders -- that is, their family members showed no other sign of autism.

The team identified 21 spontaneous mutations -- meaning they weren't inherited from either parent -- in the children's DNA. Eleven of these were mutations that would alter the protein encoded by the affected gene. In four of the 20 children, the researchers found mutations that were severe, some of which have been previously linked to autism, intellectual disability, and epilepsy.

one child had a mutation in the GRIN2B gene, which is crucial for neuronal signaling.

Developmental abnormalities in the mirror neuron system may contribute to social deficits in autism.

Now, a new study published in Biological Psychiatry reports that the mirror system in individuals with autism is not actually broken, but simply delayed.

While most of us have their strongest mirror activity while they are young, autistic individuals seem to have a weak mirror system in their youth, but their mirror activity increases with age, is normal by about age 30 and unusually high thereafter.

The results show for the first time the role of the SYN1 gene in autism, in addition to epilepsy, and strengthen the hypothesis that a deregulation of the function of synapse because of this mutation is the cause of both diseases

until now, no other genetic study of humans has made this demonstration.

The different forms of autism are often genetic in origin and nearly a third of people with autism also suffer from epilepsy.

Having sensory friendly settings is common sense and it benefits everyone, all students and learners as well as teachers and staff. Changing the classroom also teaches all students how to find practical and adaptive ways of making their setting work for them to allow for optimal learning and functioning, a skill that is beneficial to everyone. It also makes more sense to change the environment to fit the child’s needs and not the other way around. Changing the classroom helps the child with SPD blend in with other students, and it is not isolating, or stigmatizing.

A sensory friendly classroom improves attention, concentration, ability to focus for longer periods of time, learning, social functioning, and it also reduces the overall level of stress

For more specific and multiple examples of the accommodations that can be made, a book I authored titled “The Ultimate Guide to Sensory Processing Disorder” offers a comprehensive guide.