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Involvement of paraoxonase 1 genetic variants in Alzheimer’s disease neuropathology.

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Title: Involvement of paraoxonase 1 genetic variants in Alzheimer’s disease neuropathology.
Authors: Leduc, Valérie (AUTHOR), Théroux, Louise (AUTHOR), Dea, Doris (AUTHOR), Robitaille, Yves (AUTHOR), Poirier, Judes (AUTHOR)
Source: European Journal of Neuroscience. Nov2009, Vol. 30 Issue 9, p1823-1830. 8p. 3 Charts, 4 Graphs.
Subjects: Paraoxonase, Genes, Alzheimer's disease, Neurological disorders, Homeostasis
Abstract: Evidence suggests that the genes involved in brain lipid homeostasis are of particular relevance for Alzheimer’s disease (AD) etiology. Among these genes, that encoding paraoxonase 1 ( PON1) has gained newfound interest from a public health perspective, as recent studies have suggested that PON1 L55M and Q192R genetic variants might affect individual susceptibility to environmental events, such as exposure to cholinesterase inhibitors. Cholinesterase inhibitor therapy being the treatment of choice for patients with mild to moderate AD, we sought to answer two main questions: (i) are these genetic variants associated with increased AD risk, earlier age of onset/death, or shorter AD duration; and (ii) do they affect the neuropathological hallmarks of AD? This genetic study used a large cohort of clinical and autopsy-confirmed AD cases and age-matched, cognitively intact controls from the Douglas Hospital Brain Bank, Quebec, Canada ( n = 1066). The evidence presented here suggests multiple gender-specific effects of PON1 polymorphisms on AD etiopathology. The L55M Met allele exerts an AD risk-enhancing effect only in men ( P < 0.001), whereas both men and women carrying the M55M/Q192Q genotype exhibit increased survival (2.5 years, P < 0.05) and later age of onset (1.5 years, P < 0.05). These genetic variants are also individually and significantly associated, sometimes in opposite directions for both genders, with β-amyloid levels ( P < 0.001), senile plaque accumulation ( P < 0.001) and choline acetyltransferase activity ( P < 0.05) in, respectively, two of two, five of six, and three of six brain areas. These results suggest an involvement of the PON1 gene in AD etiopathology and responses to treatment. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Involvement of paraoxonase 1 genetic variants in Alzheimer’s disease neuropathology.
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  Data: &lt;searchLink fieldCode=&quot;JN&quot; term=&quot;%22European+Journal+of+Neuroscience%22&quot;&gt;European Journal of Neuroscience&lt;/searchLink&gt;. Nov2009, Vol. 30 Issue 9, p1823-1830. 8p. 3 Charts, 4 Graphs.
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– Name: Abstract
  Label: Abstract
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  Data: Evidence suggests that the genes involved in brain lipid homeostasis are of particular relevance for Alzheimer’s disease (AD) etiology. Among these genes, that encoding paraoxonase 1 ( PON1) has gained newfound interest from a public health perspective, as recent studies have suggested that PON1 L55M and Q192R genetic variants might affect individual susceptibility to environmental events, such as exposure to cholinesterase inhibitors. Cholinesterase inhibitor therapy being the treatment of choice for patients with mild to moderate AD, we sought to answer two main questions: (i) are these genetic variants associated with increased AD risk, earlier age of onset/death, or shorter AD duration; and (ii) do they affect the neuropathological hallmarks of AD? This genetic study used a large cohort of clinical and autopsy-confirmed AD cases and age-matched, cognitively intact controls from the Douglas Hospital Brain Bank, Quebec, Canada ( n = 1066). The evidence presented here suggests multiple gender-specific effects of PON1 polymorphisms on AD etiopathology. The L55M Met allele exerts an AD risk-enhancing effect only in men ( P &lt; 0.001), whereas both men and women carrying the M55M/Q192Q genotype exhibit increased survival (2.5 years, P &lt; 0.05) and later age of onset (1.5 years, P &lt; 0.05). These genetic variants are also individually and significantly associated, sometimes in opposite directions for both genders, with β-amyloid levels ( P &lt; 0.001), senile plaque accumulation ( P &lt; 0.001) and choline acetyltransferase activity ( P &lt; 0.05) in, respectively, two of two, five of six, and three of six brain areas. These results suggest an involvement of the PON1 gene in AD etiopathology and responses to treatment. [ABSTRACT FROM AUTHOR]
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  Data: &lt;i&gt;Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder&#39;s express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.&lt;/i&gt; (Copyright applies to all Abstracts.)
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      – Type: doi
        Value: 10.1111/j.1460-9568.2009.06983.x
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      – Code: eng
        Text: English
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        PageCount: 8
        StartPage: 1823
    Subjects:
      – SubjectFull: Paraoxonase
        Type: general
      – SubjectFull: Genes
        Type: general
      – SubjectFull: Alzheimer's disease
        Type: general
      – SubjectFull: Neurological disorders
        Type: general
      – SubjectFull: Homeostasis
        Type: general
    Titles:
      – TitleFull: Involvement of paraoxonase 1 genetic variants in Alzheimer’s disease neuropathology.
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            NameFull: Leduc, Valérie
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            NameFull: Théroux, Louise
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              M: 11
              Text: Nov2009
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              Y: 2009
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