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[Introduction] Down syndrome (DS) is the most common causes of mentalretardation and early Alzheimer’ disease (AD). Brain pathology of DSis characterized by reduced numberof neurons and delayed myelination. Thoughnon-neuronal cells in the brain are important for the development, survival andfunction of neurons, there is a few comparativestudies of normal development and DS fetal brains, [Methods] We observed and compared with immunoreactivityfor CD68 (marker for macrophage), HLA-DR (marker formicroglia), Olig2 (marker foroligodendrocyte)and GFAP (marker for astroglia) in the germinal matrix (GM), temporal lobe white matter (TeWM) andhippocampus from 14 weeks of gestations to newborn in 28 DS patients and 30 age-matched controls.[results] The rate of increase of CD68positive cells in the GM, CA1 hippocampal subregion and subiculumwas significantly higher in DS. Interestingly,The density of Olig2 positive cells in the GM was lower in DS brains at earlystages, then showed a transient increase contrasting controls. Olig2 expressionincreased more in the TeWM in DS.GFAP-immunoreactivity in DS was significantly lower inthe middle pregnancy period in the TeWM and did not increase between early andmiddle periods in the GM compared to controls, likely reflecting a defect inastrocyte production. [Conclusion/Discussion] Thealtered expression of non-neuronal cell markers during normal development andDS may cause the defectiveneurogenesis, leading to reduced number of neurons and delayed myelination inthe developing DS brain. This has implications for the understanding of themental retardation in DS patients.

CD68; neuropathology; HLA-DR; human; fetus; GFAP; Olig2