Increased oxidative stress in Alzheimer's disease as assessed with 4‐hydroxynonenal but not malondialdehyde

• Published in: QJM : An International Journal of Medicine 2001-09, Vol.94 (9), p.485-490
• Main Authors: McGrath, L.T., McGleenon, B.M., Brennan, S., McColl, D., McILroy, S., Passmore, A.P.
• Format: Article
• Language: English
• Subjects: Aged; Aged, 80 and over; Aldehydes - blood; Alzheimer Disease - etiology; Alzheimer Disease - metabolism; Ascorbic Acid - blood; Biological and medical sciences; Biomarkers - blood; Case-Control Studies; Chromatography, High Pressure Liquid; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; Female; Humans; Linear Models; Male; Malondialdehyde - blood; Medical sciences; Middle Aged; Neurology; Normal Distribution; Nutrition Assessment; Oxidative Stress - physiology; Psychological Tests; Spectrophotometry; Statistics, Nonparametric; Sulfhydryl Compounds - blood
• ISSN: 1460-2725; 1460-2393; 1460-2393
• DOI: 10.1093/qjmed/94.9.485

Oxidative stress is thought to play a major role in the pathogenesis of Alzheimer's disease (AD). Although there is strong post‐mortem and experimental evidence of oxidative damage occurring in AD brains, the use of markers in the peripheral circulation to show oxidative stress is less convincing. We examined plasma from AD patients for markers of increased oxidative stress. We report elevated levels of 4‐hydroxy‐nonenal (4‐HNE) in AD patients compared to controls (median 20.6, IQR 6.0–25.2 vs. 7.8, 3.3–14.5 μmol/l, respectively; p=0.001) but not malondialdehyde (MDA), and lower levels of ascorbate in AD plasma when compared to age‐matched controls (9.9, 6.0–33.7 vs. 24.2, 13.9–48.6 μmol/l; p