Abstract
Recent immunohistochemistry studies have shown increased neurogenesis in Alzheimer's diseased (AD) brains; however, the specific differential fate of AD neural progenitor cells (NPCs) is still unclear. To explore the possibilities, we have double-labeled AD and non-demented (ND) cells with an neural progenitor cells marker (NG2) and a proliferating cell marker (BrdU). The cortical NG2-expressing progenitor cells were isolated with DNA-linker cell sorting technology from rapidly autopsied (PMI < 3 h) AD and ND brains. We found that BrdU NG2+ glial progenitors are significantly increased in the AD cerebral cortex when compared to aged-matched ND brains. The neural progenitor cells isolated from both AD and ND can form clonogenic neurospheres, suggesting that the neural progenitor cells from aged brains are self-renewable. These neural progenitor cells from ND brains were able to generate both glia and neurons, while neural progenitor cells from AD brains showed a predominately glial fate. Treatment with Abeta caused the neuronal differentiation of neural progenitor cells in ND brains to decrease. The pathological environment, including the presence of Aβ, in AD brains may therefore impair the multipotential competence of neural progenitor cells. Furthermore, we also identified specific signal transduction pathways that are invivled in the neural progenitor deficits. The neural progenitor cells from aged brains are self-renewable. These s neural progenitor cells from ND brains were able to generate both glia and neurons, while neural progenitor cells from AD brains showed a predominately glial fate. Treatment with Abeta caused the neuronal differentiation of neural progenitor cells in ND brains to decrease. The pathological environment, including the presence of Abeta, in AD brains may therefore impair the multipotential competence of neural progenitor cells.
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Schedule a callMore From: Alzheimer's & Dementia: The Journal of the Alzheimer's Association
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