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

Constanze Bergt1, Takanari Nakano, Jochen Ditterich

  • 1Department of Internal Medicine, University of California, Davis, CA 95616, USA. cbergt@ucdavis.edu

Free Radical Biology & Medicine
|October 19, 2006
PubMed

Insights

Oxidative stress is linked to Alzheimer's disease (AD). Researchers found lower levels of oxidized high-density lipoprotein (HDL) in AD patients, challenging current oxidation theories and suggesting new pathways in AD pathology.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Cardiovascular Research

Background:

  • Oxidative stress is a known factor in Alzheimer's disease (AD) pathogenesis.
  • Myeloperoxidase (MPO) produces oxidants, and MPO-mediated high-density lipoprotein (HDL) oxidation is key in atherosclerosis.
  • The role of HDL oxidation in AD remains largely unexplored despite links between cardiovascular disease and AD.

Purpose of the Study:

  • To investigate the role of HDL oxidation in Alzheimer's disease.
  • To examine the relationship between myeloperoxidase (MPO), apolipoprotein A-I (apo A-I), and oxidized HDL in AD patients compared to controls.

Main Methods:

  • Quantified apolipoprotein A-I (apo A-I) and oxidized high-density lipoprotein (HDL) levels in plasma samples.
  • Compared levels between Alzheimer's disease (AD) patients and cognitively healthy, age- and gender-matched controls.

Main Results:

  • Apolipoprotein A-I (apo A-I) levels were similar between AD patients and controls (263 +/- 70 mg/dl vs. 268 +/- 70 mg/dl, p = 0.83).
  • Oxidized high-density lipoprotein (HDL) levels were significantly lower in AD patients compared to controls (4.72 +/- 1.91 U/dl vs. 6.98 +/- 3.32 U/dl, p = 0.012).
  • MPO binding to HDL was found to be dependent on the lipidation state of apo A-I.

Conclusions:

  • The observed reduction in oxidized HDL in AD patients contradicts the prevailing oxidation hypothesis.
  • Suggests that other mechanisms, such as increased antioxidant production or altered lipoprotein metabolism, may contribute to AD pathology.
  • Highlights a potential novel pathway involving HDL modification in Alzheimer's disease development.

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