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New Klimas Paper- NPY, Stress, HPA Axis and CFS

Discussion in 'XMRV Research and Replication Studies' started by shannah, Dec 29, 2010.

  1. Marco

    Marco Old blackguard

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    Near Cognac, France
    I thought I was following this until I checked one of the references.

    Wasn't the general hypothesis that Neuropeptide Y is raised in ME/CFS patients reflecting a disordered reponse to stress and that this in turn disrupts the HPA axis and leads to immune inflammation and the self reported 'emotional' symptoms?

    This line of reasoning seems to be contradicted by the following that states that NPY is anxiolytic and that "Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency" etc.

    Wouldn't high NPY levels be an appropriate response to 'stress'?



    Genetic variation in human NPY expression affects stress response and emotion.

    Zhou Z, Zhu G, Hariri AR, Enoch MA, Scott D, Sinha R, Virkkunen M, Mash DC, Lipsky RH, Hu XZ, Hodgkinson CA, Xu K, Buzas B, Yuan Q, Shen PH, Ferrell RE, Manuck SB, Brown SM, Hauger RL, Stohler CS, Zubieta JK, Goldman D.

    Laboratory of Neurogenetics, NIAAA, NIH, Bethesda, Maryland 20892, USA.

    Comment in:

    Nature. 2009 Apr 2;458(7238):E6; discussion E7.

    Abstract

    Understanding inter-individual differences in stress response requires the explanation of genetic influences at multiple phenotypic levels, including complex behaviours and the metabolic responses of brain regions to emotional stimuli. Neuropeptide Y (NPY) is anxiolytic and its release is induced by stress. NPY is abundantly expressed in regions of the limbic system that are implicated in arousal and in the assignment of emotional valences to stimuli and memories. Here we show that haplotype-driven NPY expression predicts brain responses to emotional and stress challenges and also inversely correlates with trait anxiety. NPY haplotypes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma NPY. Lower haplotype-driven NPY expression predicted higher emotion-induced activation of the amygdala, as well as diminished resiliency as assessed by pain/stress-induced activations of endogenous opioid neurotransmission in various brain regions. A single nucleotide polymorphism (SNP rs16147) located in the promoter region alters NPY expression in vitro and seems to account for more than half of the variation in expression in vivo. These convergent findings are consistent with the function of NPY as an anxiolytic peptide and help to explain inter-individual variation in resiliency to stress, a risk factor for many diseases

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