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stevedonovan t1_j83apdg wrote

Even then, the actual genetic differences (and hence protein expression) can be scattered all over the genome - only a few conditions are definitely linked to a single bad gene. There are studies which show that there are about ten genes directly implicated, and that it is mostly an inherited condition. Not an easy target for drug discovery, so mostly we put a lid on the symptoms with antipsychotic drugs, which are not fun and have neurological side effects.

Also, you can have the bad genes and not end up inflicted, just be 'functionally eccentric' or even very creative. (Not so uncommon for talented families to have the curse of madness). So, there's environment and epigenetics and all that.

Tlr;dr: the mechanisms are complex, treatment has been palliative.


Corsair4 t1_j84cu1x wrote

I was just using protein changes as an example, since that's what I'm most familiar with.

My main point was that the research techniques we use for establishing mechanisms and pathways are not compatible with humans, since they tend to be very destructive to the individual.


mojoegojoe t1_j86nu1a wrote

Exactly. What I suspect, that AI will help us vastly with data aggregation.

As these sample sets grow so to will the insite we have about how these conditions are formed. As such I believe we will alter our definition of these structures to include all the abstract interactions that go into the individual expressing the gene. We will gain better understanding as to the not so obvious, the more nunoncied structures that manufacture these symtomes like anxiety and environment.