To treat autism, I have often insisted on the importance of determining the electrical modifications, particularly the inaugural pathological event which occurs in utero. The concept of neuroarchaeology states that these initial events result in the persistence of neurons that remain immature – which do not mature and which disrupt brain functioning. We have thus done clinical trials using to treat children with ASD using a drug that has effects on immature neurons and neurons in pathological conditions but not normally in non-pathological conditions.
In this work, the authors use an animal model of mice genetically modified to express a severe genetic mutation associated with an autistic syndrome. The interesting point is that the mutation does not lead to any architectural modification of the brain but only to the electrical activity.
This work validates and extends the concept of neuroarchaeology showing how modifications – here electrical – are the cause of the syndrome and the possible target of new treatments, including when there are no structural modifications visible at this level of analysis. The initial pathological event in utero generates ionic and electrical current modifications which will persist and cause the deficits. This is valid even in a genetic syndrome, showing how, on a therapeutic level, genetics is not enough. The authors conclude: “Unfortunately, the genetic origins of autism and developmental diseases are much more complex and therapies for every combination of variants are not feasible. A big step forward in this area would be to develop a means to target phenotypes common to a multitude of etiologies, such as correcting aberrant convergent firing patterns of neurons.” Yes, but for this purpose, it is necessary to determine the modifications which occur in utero and which persist later, opening the door to effective treatment by silencing these electrical modifications.
