I am just a interested observer - I remember the issue w/ the old viral vectors were concern re longevity of the cells, i.e. the optogenetically active ones you

I am just a interested observer - I remember the issue w/ the old viral vectors were concern re longevity of the cells, i.e. the optogenetically active ones you could do experiments on for several weeks, but then they'd poop out and die off for some reason, but this was just word of mouth chitchat with a postdoc who was working on this. Not sure if this was because of the light intensity or that mutating the cell with channelrhodopsin just made it weaker in general.... granted, not sure how intense of a light you'd need; I'd think the channelrhodopsins activate w/ just a few photons at the right wavelength... Coming from the clinical/Parkinsons' disease world, if someone made a stable viral vector specific for the basal ganglia though, that would certainly help w/ one of the biggest problems of clinical DBS - after 30 years of doing this, the biggest biggest biggest problem in whether the implant will work or not is still the +/- 2mm accuracy of the stereotactic frame implanting the electrode...(no matter what surgeons/stereotactic engineers claim...)