Increased CSF F2-isoprostane concentration in probable AD

被引:201
作者
Montine, TJ
Beal, MF
Cudkowicz, ME
O'Donnell, H
Margolin, RA
McFarland, L
Bachrach, AF
Zackert, WE
Roberts, LJ
Morrow, JD
机构
[1] Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA
[2] Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA
[3] Vanderbilt Univ, Med Ctr, Dept Med, Nashville, TN 37232 USA
[4] Vanderbilt Univ, Med Ctr, Dept Psychiat, Nashville, TN 37232 USA
[5] Vanderbilt Univ, Med Ctr, Ctr Mol Neurosci, Nashville, TN 37232 USA
[6] Massachusetts Gen Hosp, Dept Neurol, Cambridge, MA USA
关键词
D O I
10.1212/WNL.52.3.562
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Objective: To quantify F-2-isoprostane levels in CSF obtained from the lumbar cistern of patients with AD, ALS, and controls. Bachground: Studies of human postmortem tissue and experimental models have suggested a role for oxidative damage in the pathogenesis of several neurodegenerative diseases, especially AD and ALS. F-2-isoprostanes are exclusive products of free-radical-mediated peroxidation of arachidonic acid that have been widely used as quantitative biomarkers of lipid peroxidation in vivo in humans. Recently, we showed that F-2-isoprostane concentrations are significantly elevated in CSF obtained postmortem from the lateral ventricles of patients with definite AD compared with controls. Methods: F-2-isoprostanes were quantified by gas chromatography/negative ion chemical ionization mass spectrometry. Results: CSF F-2-isoprostanes were increased significantly in patients with probable AD, but not in ALS patients, compared with controls. Conclusions: Increased CSF F-2-isoprostanes are not an inevitable consequence of neurodegeneration and suggest that increased brain oxidative damage may occur early in the course of AD.
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页码:562 / 565
页数:4
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