Haydar, Tarik F PHD
Boston University Medical Campus
Boston University Medical Campus
Gallo, VittorioHaydar, Tarik F
The novel understanding of oligodendrocyte maturation defects in brains of humans with Down syndrome and the Ts65Dn mouse model open a new avenue to possible cognitive therapies for persons with Down syndrome—we have shown that these cellular defects lead to less myelin in the forebrain and cerebellum and that this causes slower neuronal transmission in the brain. The experiments in this proposal are designed to uncover the cell intrinsic and extrinsic mechanisms underlying the cellular defect and to measure whether motor and/or spatial learning and memory are correlated with the dysmyelination. Finally, we will investigate genetic and pharmacological therapies designed to promote myelination and improve cognitive and motor function.