Premium
Chronic exposure to U18666A is associated with oxidative stress in cultured murine cortical neurons
Author(s) -
Koh Chor Hui Vivien,
Whiteman Matthew,
Li QiaoXin,
Halliwell Barry,
Jenner Andrew M.,
Wong Boon Seng,
Laughton Katrina M.,
Wenk Markus,
Masters Colin L.,
Beart Philip M.,
Bernard Ora,
Cheung Nam Sang
Publication year - 2006
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2006.03958.x
Subject(s) - oxidative stress , pathogenesis , apoptosis , neurodegeneration , neuroscience , disease , biology , secretion , alzheimer's disease , cortical neurons , medicine , endocrinology , biochemistry
Findings that antioxidant treatment may be beneficial in Alzheimer's disease indicate that oxidative stress is an important factor in its pathogenesis. Studies have also suggested that cholesterol imbalance in the brain might be related to the development of neurological disorders. Previously, we have reported that U18666A, a cholesterol transport‐inhibiting agent, leads to apoptosis and intracellular cholesterol accumulation in primary cortical neurons. In this study, we found that neuronal apoptosis mediated by U18666A is associated with oxidative stress in the treated cortical neurons. Cortical neurons treated with U18666A also showed decreased secretion and increased intraneuronal accumulation of β‐amyloid. The association of neuronal apoptosis with oxidative stress and Aβ accumulation may provide clues to the pathogenesis of Alzheimer's disease, as well as the role oxidative stress plays in other neurodegenerative diseases.