> Is this study important because they found the gene (or a gene?) that corresponds to that?
The paper only concludes that the gene is inactive when there's demyelination, the paper doesn't actually say that it causes it.
The previous research I've read says that it is expressed during repair (i.e it is the repair tool, so is in play during repair of the cells).
So even for those of us who have GPR17, making sure it is expressed for repair (if it does repair) would mean a longer active brain life.
I've got half-a binder full of research on PRRT2 from a family incident & then the opposite with conductivity research for SCN1A.
The developmental myelination defects are really weird to read about, because if they are about expression rather than presence of a gene & often a single CNV doesn't mean anything (or everything, argh), the environmental factors overwhelm things ("what kind of fat and how much did you eat during your childhood synaptic pruning period").
The paper only concludes that the gene is inactive when there's demyelination, the paper doesn't actually say that it causes it.
The previous research I've read says that it is expressed during repair (i.e it is the repair tool, so is in play during repair of the cells).
So even for those of us who have GPR17, making sure it is expressed for repair (if it does repair) would mean a longer active brain life.
I've got half-a binder full of research on PRRT2 from a family incident & then the opposite with conductivity research for SCN1A.
The developmental myelination defects are really weird to read about, because if they are about expression rather than presence of a gene & often a single CNV doesn't mean anything (or everything, argh), the environmental factors overwhelm things ("what kind of fat and how much did you eat during your childhood synaptic pruning period").