Get access

Dietary lipids and their oxidized products in Alzheimer's disease

Authors

  • Laura Corsinovi,

    1. Internal Medicine Division, Cardinal Massaia Hospital, Asti, Italy
    2. Department of Cardiology, University of Turin, Turin, Italy
    Search for more papers by this author
  • Fiorella Biasi,

    Corresponding author
    1. Department of Clinical and Biological Sciences, University of Turin at San Luigi Gonzaga Hospital, Orbassano (Turin), Italy
    • Department of Clinical and Biological Sciences, University of Turin at San Luigi Gonzaga Hospital, 10043 Orbassano (Turin), Italy Fax: +39-0116-705424
    Search for more papers by this author
  • Giuseppe Poli,

    1. Department of Clinical and Biological Sciences, University of Turin at San Luigi Gonzaga Hospital, Orbassano (Turin), Italy
    Search for more papers by this author
  • Gabriella Leonarduzzi,

    1. Department of Clinical and Biological Sciences, University of Turin at San Luigi Gonzaga Hospital, Orbassano (Turin), Italy
    Search for more papers by this author
  • Gianluca Isaia

    1. Geriatric Division, University of Turin at San Luigi Gonzaga Hospital, Orbassano (Turin), Italy
    Search for more papers by this author

Abstract

Alzheimer's disease (AD) is the commonest form of dementia in the elderly, characterized by memory dysfunction, loss of lexical access, spatial and temporal disorientation, and impaired judgment. A growing body of scientific literature addresses the implication of dietary habits in the pathogenesis of AD. This review reports recent findings concerning the modulation of AD development by dietary lipids, in animals and humans, focusing on the pathogenetic role of lipid oxidation products. Oxidative breakdown products of ω-6 polyunsaturated fatty acids (ω-6 PUFAs), and cholesterol oxidation products (oxysterols), might play a role in favoring β-amyloid deposition, a hallmark of AD's onset and progression. Conversely, ω-3 PUFAs appear to contribute to preventing and treating AD. However, high concentrations of ω-3 PUFAs can also produce oxidized derivatives reacting with important functions of nervous cells. Thus, altered balances between cholesterol and oxysterols, and between ω-3 and ω-6 PUFAs must be considered in AD's pathophysiology. The use of a diet with an appropriate ω-3/ω-6 PUFA ratio, rich in healthy oils, fish and antioxidants, such as flavonoids, but low in cholesterol-containing foods, can be a beneficial component in the clinical strategies of prevention of AD.

Get access to the full text of this article

Ancillary