neurons in which the disease becomes manifest. Specifically, even if disease such as Parkinson’s or Huntington’s disease manifest in a dysfunction of dopaminergic or striatal neurons, respectively, this manifestation likely represents a particular vulnerability of specific types of neurons to a general disease process, and not a disease process that is restricted to these types of neurons. Thus, even for such diseases it may not only be feasible, but actually be productive to examine Ngn2-generated iN cells as a homogeneous population of glutamatergic neurons, especially in co-culture with mouse neurons or after transplantation into the mouse brain.
