Down Syndrome, a genetic disorder resulting from trisomy of chromosome 21, is frequently associated with neurodevelopmental anomalies and vascular and hematologic pathologies. Moreover, the predisposition of Down Syndrome patients to develop early onset Alzheimer's disease post 50 years of age has been postulated to be linked with the trisomy state of the amyloid precursor protein gene located on chromosome 21. However, the pathogenesis of Alzheimer's disease remains elusive since the accumulation of amyloid beta does not necessarily cause Alzheimer's disease, and antibody therapy aimed at removing amyloid beta does not achieve remission. Recent literature has provided intriguing evidence indicating the amelioration of cognitive function in geriatric mice upon administration of plasma from younger cohorts (Castellano et al., Nature, 2017), implicating a potential connection between cerebrovascular and hematologic conditions and insinuating that blood components may exert influence on cerebral function. Consequently, this study is designed to investigate whether the transplantation of bone marrow cells from Down Syndrome model mice leads to alterations in brain functionality. In this presentation, we will present data obtained to date and discuss potential mechanisms that regulate brain function by the hemopoietic stem cell.