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  • 2000-2004  (3)
  • 1
    Electronic Resource
    Electronic Resource
    Apolipoprotein E isoforms and apolipoprotein AI protect from amyloid precursor protein carboxy terminal fragment-associated cytotoxicity (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 91 (2004), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Inheritance of the apolipoprotein (APO) E gene ɛ4 or ɛ2 allele alters the risk of developing Alzheimer disease (AD), while increased alpha-tocopherol (AT) intake appears to lower the risk of AD. As APOE is a major apolipoprotein in the CNS and AT in vivo is transported in lipoproteins, we tested the hypothesis that CNS lipoproteins, as modeled by relevant concentrations of high density lipoprotein (HDL), and AT would interact to suppress neurotoxicity in a cell culture model of amyloid beta (Aβ)- related toxicity. These cells conditionally express C99-derived peptides, proposed to be a key step in AD pathogenesis; this expression is closely associated with subsequent cell death. We found that physiologic concentrations of lipoproteins present in the CNS protected from C99-associated toxicity and provided evidence for two mechanisms of protection. The first was AT-independent, APOE isoform-dependent, and most potent for the APOE2 isoform. The second was a synergistic protection afforded by a combination of APOAI, or less so APOE, and AT. These data provide a novel explanation for the apparent AD-protective effect of inheriting an ɛ2 APOE allele, and suggest that optimizing AT enrichment of CNS lipoproteins or devising APOAI mimetics may augment AT efficacy in treating AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02818.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Lessons from human progeroid syndromes (2000)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 408 (2000), S. 263-266 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] A number of human genes have been identified in which mutations can lead to the accelerated emergence of features of senescence. Studies of these genes, and of the functions of their protein products, may lead to a clearer understanding of the nature of senescence, and could provide clues for ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/35041705
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Ageing Mice and mitochondria (2004)
    [s.l.] : Nature Publishing Group
    Nature 429 (2004), S. 357-359 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Mitochondria are little pockets of energy within cells, shouldering the important task of converting food into usable energy forms. To meet demands, every cell contains thousands of them. Unlike most other cellular compartments, mitochondria have their own genomes, which encode a few mitochondrial ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/429357a
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    Paper (German National Licenses)
    Fulltext
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