Neurodevelopmental Disorder Quotes

In 2010, the psychiatrist Thomas Insel, then director of NIMH, called for the research community to redefine schizophrenia as “a collection of neurodevelopmental disorders,” not one single disease. The end of schizophrenia as a monolithic diagnosis could mean the beginning of the end of the stigma surrounding the condition. What if schizophrenia wasn’t a disease at all, but a symptom? “The metaphor I use is that years ago, clinicians used to look at ‘fever’ as one disease,” said John McGrath, an epidemiologist with Australia’s Queensland Centre for Mental Health Research and one of the world’s authorities on quantifying populations of mentally ill people. “Then they split it into different types of fevers. And then they realized it’s just a nonspecific reaction to various illnesses. Psychosis is just what the brain does when it’s not working very well.

ADHD is a neurodevelopmental disorder, which means the nervous system, including the brain, develops and functions differently.

a common neurodevelopmental disorder that significantly affects a person’s ability to focus and maintain attention. It affects behavior, mood, and executive functions. Simply put, people with ADHD have a constant need for stimuli. In other words, ADHD is a brain-wiring disorder, not a disease. In a person with ADHD, the brain’s wiring is slightly different from others, and the brain prioritizes tasks differently (Sinfield,

Children do not develop what is called the “theory of mind” until ages three to five. Theory of mind is said to be present when someone is able to understand that other people have conscious thoughts and behaviors independent of them. Theory of mind is necessary for empathy and most social interactions—it’s how you understand someone else’s perspective and thinking process. Children who struggle to develop theory of mind are often diagnosed as being on the autism spectrum or having schizophrenia, ADHD, or some other problem. See B. Korkmaz, “Theory of Mind and Neurodevelopmental Disorders in Childhood,” Pediatric Research

Tourette’s syndrome is a neurodevelopmental disorder where the patient frequently suffers from involuntary convulsive movements (tics) which in some cases are associated with involuntary swearing. Two unrelated individuals with this disorder were shown to have the same single base change in the 3′ UTR of a gene called SLITRK139. SLITRK1 appears to be required for neuronal development. The base change in the Tourette’s patients introduced a binding site for a short ncRNA called miR-189. This suggests that SLITRK1 expression may be abnormally down-regulated via such binding, at critical points in development. This alteration is only present in a few cases of Tourette’s but raises the tantalising suggestion that mis-regulation of miRNA binding sites in other neuronal genes may be involved in other patients.

Exposure to Thimerosal increased beginning in 1989 and rose sharply during the early 1990s as new vaccines were added to the US childhood vaccine schedule. This increased exposure to mercury via vaccines coincided closely with increased case reports of neurodevelopmental disorders, including a dramatic increase in autism spectrum disorder (ASD) cases and a rise in attention deficit hyperactivity disorder (ADHD).

the trauma field is still early in the process of clearly differentiating between post-traumatic stress disorder (PTSD) and complex post-traumatic stress disorder (C-PTSD). A distinguishing factor of C-PTSD is the focus on self-organization, which refers to a neurodevelopmental and psychobiological process of shaping one’s personality and life experience. C-PTSD focuses on three areas of disturbances in self-organization: emotional regulation, self-concept, and relationships.

It is also important to note that not all pathological presentations are caused by the environment. A child may have underlying difficulties such as intellectual disabilities or other neurodevelopmental disorders. On the other hand, just because a child has survived unscathed does not mean that the environment was benign. We know that some children are naturally less sensitive to environmental influences and as such are more resilient to harsh environments.

In the early 2000s this idea of synaptic pruning was well established, but how the process actually occurred was a bit of a mystery. In 2007 Beth Stevens, a postdoctoral scientist working in the late Ben Barres’s lab at Stanford University, found a very unexpected answer. In the immune system, specific immune molecules called complement proteins attach themselves to microbes or damaged cells and act as an ‘EAT ME!’ signal to macrophages. Beth found that mice that lacked complement proteins were unable to prune their synapses.18 A few years later, in 2013, after Beth Stevens had moved to Boston Children’s Hospital to start her own lab, she and her postdoctoral fellow Dorothy Schafer found that once these unused synapses are coated in complement proteins, microglia turn up to engulf and destroy them (like coating any food in chocolate sauce when there’s a young child in the vicinity).19 Stevens’s team later found that the synapses that are in regular use produce a ‘DON’T EAT ME!’ signal (like covering a child’s meal in kale).20 Microglia are not just the brain’s equivalent of macrophages, they are the sculptors of our brains. If microglia are to be renamed – a suggestion made by some, as they are not true glial cells – my suggestion would be ‘microangelos’. Although, somehow, I don’t see that catching on. Microglia’s role in synaptic pruning may also have significant relevance for developmental disorders. Abnormalities in neuronal pruning can be seen in subsets of people with neurodevelopmental conditions such as schizophrenia. While we don’t yet know exactly how these alterations in brain connectivity manifest in disease, there is hope that treatments targeting microglia and complement proteins may one day be of great use.