I have a great interest in evolution. The concept that seemed so simple when discovered , it was a wonder how naturalists had not come across it sooner. The basic principle of evolution by natural selection is that a very simple process could account for so much complexity. Looking at a living animal , it was impossible to fathom how an event could account for such a giant leap. Of course our mental biases saw this as a single event rather than minute steps taken over milions of years. It could well be possible that there is a simple genetic mutation or enviromental phenomenon that could have a knock on effect , on say the , process of embryology , through childhood and onto adulthood. When we come to look at schizophrenia we usually do at its presentation , at which stage the disease has developed beyond its basic pathology , incrementally adding more and more complexity in terms of its definition.

For example there is a hypothesis I read that neuron migration from deep brain, out to the cerebrum in embryology and early childhood could account for the differing and varying symptoms you see in psychotic presentation. Just because the symptoms differ that does not mean there is not a basic underlining pathology at fault. Again how the brain stem , cerebral cortex, hind brain , mid brain fore brain develop , is essential like an opening flower with neuron migration pushing outwards to form the cortex. Such is the complexity and uniqueness of this migration it could well be responsible for all kinds of varying symptoms as characterised by the migration towards and formation of the cortex.

Just an idea.

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Yeah there are definitely some theories that go back to development and some which use epigenics which is transient changes in expression so it could be anything. But I guess what I was saying here is that you and I probably have different mutations that have the same net outcome...this is like the third or fourth study like this where all of the suspected mutations are in fact rare...like I know somebody specifically studied the d2 receptor and found variations in some sz patients and there are also copy number variants and snps for gwas studies. I personally have two copies of a rare mutation in the metabotropic glutamate receptor grm3 which regulates levels of glutamate at the synapse thus altering nmda activity...it has a 0.0% frequency in the population(for two copies...10% for one but clearly that's not in equilibrium or you would expect like 2.5% for the double).

I had to look up knock on effect....it's not a common US expression...at first I thought you meant that we had a gain of function like psychic abilities or something.