What does that even mean – “A connection between autism and concussions?” Well, recently I’ve learned about the neurochemistry behind what occurs in the brains of autistic patients and found that the root of the problem is simply too many networks, signals, or connections in the brain, which leads to overstimulation of the brain. Obviously that’s very simplified, but at the root that is the problem.
In the case of a concussion, the root cause is a little broader. The trauma the brain experiences leads to many things going wrong. These include oxidative stress and anatomical deficiencies in the structure of the neurons. Specifically, the axons of the neuron are literally “broken,” which leads to a lack of networking in the brain and, subsequently, things going wrong in the longterm if the concussive patient isn’t given adequate rehabilitation time.
There’s the connection – the brains of patients with autism and those experiencing concussions are basically the opposite, in terms of axonal connections. Interesting, right? Well, recently, I’ve done research in the area of axonal sprouting and targeting the neurochemical pathway – PI3K-AKT – that is involved in autism. If this pathway is “turned on” too often, or not inhibited enough, autistic behaviors are observed in test subjects. However, a molecule responsible for inhibiting this pathway – phosphate and tensin homolog (PTEN) – is also an interest of mine in potentially treating brain injuries like concussions. If PTEN can be inhibited, the negative outcomes of a concussion can be better controlled. Below is a simplified schematic outlining this idea.
Following binding of a ligand to the tyrosine kinase receptor on the membrane of the cell, PTEN inhibits PI3K signaling by dephosphorylating the lipid signaling intermediate PIP(3), which is a necessary factor in the communication between PI3K and AKT. This dephosphorylation prevents the pathway from promoting cell survival and inhibiting apoptosis, or programmed cell death.
However, if PTEN is inhibited, PI3K-AKT is turned on even more, which will lead to more axonal sprouting and more networking. So, would this PTEN inhibition lead to autistic behaviors, then? Or would a potential treatment for concussion lead to promising results with little drawbacks? That’s a question that has yet to be answered. But, like many areas of neuroscience, it interests me significantly. Obviously this idea that autism and concussions are somehow related is very broad and not understood well, but nonetheless, I believe it deserves some attention.
Neuronal Networking – A Connection Between Autism and Concussions?
