ways to access the brain own plasticity and has demonstrated over and over seemingly miraculous transformations. She says, “When the brain gets information it needs it will organize that information . . . [and it] starts forming new connection at a ridiculously fast pace.”
<17:36 they move and you’re there when they move
17:50 in order to form patterns … open the conversation, get new information
All kids want to be successful. But some don’t know better options.
Hit the table. Hit it harder. They learn the difference.
I had constructed this fantasy in my mind about disability and I had thought to myself, because I can’t read unspoken cues from other people, that I am missing all of these messages of beauty and sweetness and light, and if only I could see those things, my life would be immeasurably better. But when the ability to see into people came on …
TMS actually changed how I saw my memories as a child. I now remember times when people were laughing, but now thanks to TMS, I realize they were laughing at me.
ASD is identified by two primary diagnostic markers: difficulties in social communication and restricted or repetitive behaviors and interests.
Examples of difficulties in social communication include challenges in social reciprocity, nonverbal social behaviors, and establishment of social relationships. Restrictive and repetitive behaviors include stereotypic behavior or speech, excessive adherence to routines, and highly fixated interests.
ASD is diagnosed about three times more frequently in boys than in girls. Intellectual disability was once thought to be a condition that typically accompanied ASD; however, current estimates are that 35% of individuals with ASD score above the IQ cutoff (i.e., around 70 depending on the test) for intellectual disability (Dykens & Lense, 2011).
Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis.
Lancet. 2013 Apr 20;381(9875):1371-9. http://www.ncbi.nlm.nih.gov/pubmed/23453885
Cross-Disorder Group of the Psychiatric Genomics Consortium.
Erratum in: Lancet. 2013 Apr 20;381(9875):1360.
Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories.
We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.
We analyzed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders
SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10(-8)) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2.
Model selection analysis supported effects of these loci for several disorders.
Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity.
Pathway analysis supported a role for calcium channel signalling genes for all five disorders.
Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology.
These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.
This article presents our discovery that intranasal administration of oxytocin enhances activity in the brain for socially meaningful stimuli and attenuates its response to nonsocially meaningful stimuli in children with autism spectrum disorder (ASD) as measured via functional MRI. We also identified a relationship between changes in salivary oxytocin following administration and enhancements in brain function.
These discoveries are particularly important given the urgent need for treatments that target the core social dysfunction in ASD. The functional neural attunement we demonstrated might facilitate social learning, thus potentially bringing about long-term change in neural systems and subsequent behavioral improvements.
Our results illustrate the power of a translational neuroscience approach to facilitate the development of pharmacological interventions for neurodevelopmental disorders like ASD.
Serotonin and vitamin D have been proposed to play a role in autism; however, no causal mechanism has been established.
Here, we present evidence that vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues outside the blood-brain barrier at a distinct VDRE.
The proposed mechanism explains 4 major characteristics associated with autism:
the low concentrations of serotonin in the brain and its elevated concentrations in tissues outside the blood-brain barrier;
the low concentrations of the vitamin D hormone precursor 25-hydroxyvitamin D [25(OH)D3];
the high male prevalence of autism;
and the presence of maternal antibodies against fetal brain tissue.
Two peptide hormones, oxytocin and vasopressin, are also associated with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and the arginine vasopressin receptor contain VDREs for activation. Supplementation with vitamin D and tryptophan is a practical and affordable solution to help prevent autism and possibly ameliorate some symptoms of the disorder.