Oxidative stress, linked to Abeta-lipid interactions, plays a pathogenetic role in Alzheimer's disease. We investigated modifications of lipid peroxidation products in plasma of 52 AD patients, 42 healthy controls and 16 patients with amyotrophic lateral sclerosis, a neurodegenerative disease where oxidative stress also plays a pathogenetic role. Final lipid peroxidation products were measured in plasma by thiobarbituric acid reactive substances (TBARS) assay before and after ex vivo oxidative stress catalysed by copper. There were no significant changes at basal conditions, but after copper-induced oxidation TBARS levels were higher in AD patients (19.0 microM +/- 2.2) versus both controls (5.2 microM +/- 0.8, p<0.001) and ALS patients (7.6 microM +/- 2.1, p<0.01). Stimulated TBARS levels were significantly higher in mild and moderate AD (p<0.0001) with respect to controls, but not in severe AD patients, with a significant inverse correlation between disease severity and lipid peroxidation (p<0.005, r2=0.21). Treatment of a subgroup (13) of mild and moderate AD patients with vitamin C and E for three months decreased plasma lipoperoxidation susceptibility by 60%. Thus, oxidative stress, expressed as ex vivo susceptibility to lipid peroxidation, appears to be an early phenomenon, probably related to AD pathogenetic mechanisms.

Galbusera, C., Facheris, M., Magni, F., Galimberti, G., Sala, G., Tremolada, L., et al. (2004). Increased susceptibility to plasma lipid peroxidation in Alzheimer disease patients. CURRENT ALZHEIMER RESEARCH, 1(2), 103-109 [10.2174/1567205043332171].

Increased susceptibility to plasma lipid peroxidation in Alzheimer disease patients

GALBUSERA, CARMEN;FACHERIS, MAURIZIO;MAGNI, FULVIO;GALIMBERTI, GLORIA;SALA, GESSICA;TREMOLADA, LUCIA;ISELLA, VALERIA;APPOLLONIO, ILDEBRANDO;KIENLE, MARZIA DONATELLA;FERRARESE, CARLO
2004

Abstract

Oxidative stress, linked to Abeta-lipid interactions, plays a pathogenetic role in Alzheimer's disease. We investigated modifications of lipid peroxidation products in plasma of 52 AD patients, 42 healthy controls and 16 patients with amyotrophic lateral sclerosis, a neurodegenerative disease where oxidative stress also plays a pathogenetic role. Final lipid peroxidation products were measured in plasma by thiobarbituric acid reactive substances (TBARS) assay before and after ex vivo oxidative stress catalysed by copper. There were no significant changes at basal conditions, but after copper-induced oxidation TBARS levels were higher in AD patients (19.0 microM +/- 2.2) versus both controls (5.2 microM +/- 0.8, p<0.001) and ALS patients (7.6 microM +/- 2.1, p<0.01). Stimulated TBARS levels were significantly higher in mild and moderate AD (p<0.0001) with respect to controls, but not in severe AD patients, with a significant inverse correlation between disease severity and lipid peroxidation (p<0.005, r2=0.21). Treatment of a subgroup (13) of mild and moderate AD patients with vitamin C and E for three months decreased plasma lipoperoxidation susceptibility by 60%. Thus, oxidative stress, expressed as ex vivo susceptibility to lipid peroxidation, appears to be an early phenomenon, probably related to AD pathogenetic mechanisms.
Articolo in rivista - Articolo scientifico
Alzheimer disease, lipid peroxidation, Aged; Amyotrophic Lateral Sclerosis; Antioxidants; Apolipoproteins E; Ascorbic Acid; Case-Control Studies; Copper; Female; Humans; Male; Middle Aged; Oxidation-Reduction; Polymorphism, Genetic; Severity of Illness Index; Thiobarbituric Acid Reactive Substances; Vitamin E
English
103
109
7
Galbusera, C., Facheris, M., Magni, F., Galimberti, G., Sala, G., Tremolada, L., et al. (2004). Increased susceptibility to plasma lipid peroxidation in Alzheimer disease patients. CURRENT ALZHEIMER RESEARCH, 1(2), 103-109 [10.2174/1567205043332171].
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/11908
Citazioni
  • Scopus 52
  • ???jsp.display-item.citation.isi??? 48
Social impact