Investigating Pathomechanisms of Neurodevelopmental and Neuropsychiatric Diseases Using Human Cell Models

[Hugo Sanchez-Castillo]

One of the most extraordinary fields in research is modelate the neurodegenerative and neurodevelopment human disease like schizophrenia, autism, parkinson, etc. In this wonderful session we learn about how this models are doing right now. However there is some questions that we will consider. What happened with the microglial systems through this mutations?, the microglial systems adapt it in the same speed or even what if the microglial systems buffered some of the effects of the mutations?. Is well know that the microglia receives information from the neurons and those information can release the gliotransmitters. What about this molecules?, there is change in the way in which the glial cells communicate between them? How the migratory dynamics change between species?. In the first topic of this session one of the conclusions it was that after the manipulations we observed a disorganization of the cells, however I was wonder if we were in front of a new organization, what if al of this other cells are responding organization itself in a different way?. Under this, we need to check twice if we have a new form of organization derivated from all this manipulations and that point of view make sense if we consider that in the neurodegenerative and neurodevelopmental diseases the SNC have to find new ways to adapt to the abnormal condition. 

The second talk introduces us to the schizophrenic modeling, particularly modulating synaptic proteins which it could be affected not only in schizophrenia but in autism. However is well know that there is many similarities between schizophrenia and bipolar disorder and major depression, and under this circumstances  what happened if we consider this diseases in the proposed model? we will find something?, behaviourally speaking, what we should spect about this models?... We have to remind that schizophrenia have the cognitive symptomatology as one of most prevalent symptoms in  this patients even when the negative and positive symptoms are diminished the cognitive symptom prevails. Finally is important to think how the drugs could act in this models.

All this questions were popping thanks to this remarkable speakers and is clear for me that we have so much to learn and to improve in our actual models.