Oxidized plasma high-density lipoprotein is decreased in Alzheimer's disease

Constanze Bergt, Takanari Nakano, Jochen Ditterich, Charles DeCarli, Jason P. Eiserich

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD), and the enzyme myeloperoxidase (MPO) has been identified as one source of reactive oxidants. MPO-mediated oxidation of high-density lipoprotein (HDL) plays an important role in the pathogenesis of atherosclerosis and although several links between cardiovascular disease and AD have been reported, surprisingly little is known about the role of HDL oxidation in AD. We show that MPO binding to isolated HDL depends on the lipidation state of apolipoprotein A-I (apo A-I), the major protein constituent of HDL. When quantifying apo A-I and oxidized HDL in plasma of AD patients and cognitive healthy, age- and gender matched controls, we observed similar apo A-I levels in AD patients (263 ± 70 mg/dl) and controls (268 ± 70 mg/dl, p = 0.83). In striking contrast, oxidized HDL was significantly reduced in AD patients (4.72 ± 1.91 U/dl) compared to controls (6.98 ± 3.32 U/dl, p = 0.012). The marked decrease of oxidized HDL in AD patients is surprising considering the current oxidation hypothesis. We suggest that additional mechanisms, including increased antioxidant production and/or altered lipoprotein metabolism, might be involved in AD pathology.

Original languageEnglish (US)
Pages (from-to)1542-1547
Number of pages6
JournalFree Radical Biology and Medicine
Issue number10
StatePublished - Nov 15 2006


  • Apolipoprotein A-I
  • Myeloperoxidase
  • Neurodegenerative disease
  • Oxidative stress

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry


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