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자료유형
학술저널
저자정보
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제37권 제6호
발행연도
2005.1
수록면
559 - 566 (8page)

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Amyloid β (Aβ) neurotoxicity is believed to play a critical role in the pathogenesis of Alzheimer's disease (AD) mainly because of its deposition in AD brain and its neuronal toxicity. However, there have been discrepancies in Aβ-induced cytotoxicity studies, depending on the assay methods. Com-β42-induced in vitro cyto-toxicity might be useful to elucidate the etiological role of Aβ in the pathogenesis of AD. In this study, MTT, CCK-8, calcein-AM/EthD-1 assays as well as thorough microscopic examinations were compara-tively performed after Aβ42 treatment in a neuronal precursor cells (NT2) and a somatic cells (EcR293). Extensive formation of vacuoles was observed at the very early stage of Aβ42 treatment in both cells. Early observation of Aβ42 toxicity as seen in vacuole formation was also shown in MTT assay, but not in CCK-8 and calcein-AM/EthD-1 assays. In addition, Aβ42 treatment dramatically accelerated MTT for-mazan exocytosis, implying its effect on the ex-tensive formation of cytoplasmic vacuoles. Aβ42 seems to cause indirect inhibition on the intracellular MTT reduction as well as vacuole formation and exocytosis enhancement. Following the acute cellular dysfunction induced by Aβ42, the prolonged treatment of micromolar concentration of Aβ42 resulted in slight inhibition on redox and esterase activity. The early Aβ42-induced vacuolated mor-phology and later chronic cytotoxic effect in neuronal cell might be linked to the chronic neurode-generation caused by the accumulation of Aβ42 in AD patients' brain.

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