Chronic exposure to U18666A is associated with oxidative stress in cultured murine cortical neurons
- Author(s)
- Koh, CHV; Whiteman, M; Li, QX; Halliwell, B; Jenner, AM; Wong, BS; Laughton, KM; Wenk, M; Masters, CL; Beart, PM; Bernard, O; Cheung, NS;
- Details
- Publication Year 2006-08,Volume 98,Issue #4,Page 1278-1289
- Journal Title
- JOURNAL OF NEUROCHEMISTRY
- Publication Type
- Journal Article
- Abstract
- 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 beta-amyloid. The association of neuronal apoptosis with oxidative stress and A beta accumulation may provide clues to the pathogenesis of Alzheimer's disease, as well as the role oxidative stress plays in other neurodegenerative diseases.
- Publisher
- BLACKWELL PUBLISHING
- Keywords
- TRANSGENIC MOUSE MODEL; AMYLOID BETA-PEPTIDE; ALZHEIMERS-DISEASE; LIPID-PEROXIDATION; CELL-DEATH; NEURODEGENERATIVE DISEASES; PROTEIN OXIDATION; PROTEASOME FUNCTION; DNA-DAMAGE; CHOLESTEROL
- Publisher's Version
- https://doi.org/10.1111/j.1471-4159.2006.03958.x
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2006-08-01 12:00:00