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Apolipoprotein E and cognitive performance

Author

Listed:
  • Jacob Raber

    (Gladstone Institute of Neurological Disease, University of California
    University of California)

  • Derek Wong

    (Gladstone Institute of Neurological Disease, University of California)

  • Gui-Qiu Yu

    (Gladstone Institute of Neurological Disease, University of California)

  • Manuel Buttini

    (Gladstone Institute of Neurological Disease, University of California
    University of California)

  • Robert W. Mahley

    (Gladstone Institute of Neurological Disease, University of California
    Cardiovascular Research Institute, University of California
    University of California
    University of California)

  • Robert E. Pitas

    (Gladstone Institute of Neurological Disease, University of California
    Cardiovascular Research Institute, University of California
    University of California)

  • Lennart Mucke

    (Gladstone Institute of Neurological Disease, University of California
    University of California
    Neuroscience Program, University of California)

Abstract

Key proteins implicated in the development of Alzheimer's disease are the β-amyloid precursor protein, which gives rise to the β-amyloid peptides that accumulate in the deteriorating brain1,2, and the different isoforms of apolipoprotein E (apoE). The apoE4 variant increases the risk of developing the disease compared with apoE3 (ref. 3). We have tested the spatial memory of transgenic mice carrying human forms of these proteins and find that it is impaired in mice with apoE4 but not those with apoE3, even though the levels of β-amyloid in their brains are comparable. The fact that apoE3, but not apoE4, can protect against cognitive deficits induced by β-amyloid may explain why human apoE4 carriers are at greater risk of developing Alzheimer's than apoE3 carriers.

Suggested Citation

  • Jacob Raber & Derek Wong & Gui-Qiu Yu & Manuel Buttini & Robert W. Mahley & Robert E. Pitas & Lennart Mucke, 2000. "Apolipoprotein E and cognitive performance," Nature, Nature, vol. 404(6776), pages 352-354, March.
    • Handle: RePEc:nat:nature:v:404:y:2000:i:6776:d:10.1038_35006165
    DOI: 10.1038/35006165
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