A malfunctioning gene within the thalamus region of the brain may be responsible for sensory overload and the symptoms associated with it, according to researchers
Sensory overload is responsible for attention deficits, aggression and trouble sleeping – symptoms frequently associated with autism, ADHD and similar conditions.
The study, published in the journal Nature, focuses on the role of a gene called PTCHD1 within the thalamus, the section of the brain that relays input from the eyes, ears, and skin to the cortex, where it is processed further before driving behaviour.
There is evidence that within the thalamus PTCHD1 helps prioritise important sights and sounds, filtering out distracting sensory inputs. Previous studies have shown that people born with defects in the PTCHD1 gene struggle with sensory overload, as background ‘noise’ leaks into consciousness.
For the newly published study, the research team from NYU Langone Medical Center in New York and Massachusetts Institute of Technology genetically engineered mice to lack the PTCHD1 gene. They then measured the ability of their ‘PTCHD1 knockout’ mice to perform tasks that required them to discern between light flashes linked to a food reward and distractions (no reward) when compared to normal mice. By switching the stimulus linked to rewards, the tasks forced the mice to reconsider how much attention they paid to each flash as researchers monitored nerve circuit signalling patterns.
The study found that mice without PTCHD1 cannot tune out distractions as well as their normal counterparts. The researchers also defined the mechanisms behind these deficits and partly reversed them with an experimental drug called 1-ethyl-2-benzimidazolinone.
To our knowledge, this is the first study to detail the biology behind thalamic dysfunction in cognitive disorders caused by PTCHD1 defects in the mammalian brain. We believe that this work defines a new disease category based on common biological signatures surrounding the “leaky thalamus” and based on a dysfunctional thalamic reticular nucleus.
Said study senior investigator Michael Halassa, MD, PhD, an assistant professor at the Neuroscience Institute at NYU Langone.