Studies in mice suggest that Olig2 gene dosage alters cerebral cortical interneuron development and contributes to trisomy-21/Down-syndrome-related intellectual disability.Xu et al.
These findings suggest that OLIG2 over-expression inhibits neural progenitor proliferation through changes in potassium channel activity, thereby contributing to the reduced neuronal numbers and brain size in DS.
A new study finds that the expression of two affected genes, Olig1 and Olig2, is critical for maintaining the balance of inhibitory and excitatory signaling in a mouse model of Down syndrome.
BHLHB1 mapped to the region of chromosome 21 that has been proposed to be responsible, at least in part, for the learning deficits seen in children with Down's syndrome.