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Hippocampus vol in schizophrenia

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    Post by Pivalde on ymb along with some relevant replies...

    pivalde • Feb 10, 2015 2:17 PM

    Hippocampus vol in schizophrenia
    PLoS One. 2015 Feb 6;10(2):e0117785. doi: 10.1371/journal.pone.0117785. eCollection 2015.

    Hippocampal subfield volumes in first episode and chronic schizophrenia.

    Kawano M1, Sawada K2, Shimodera S1, Ogawa Y3, Kariya S4, Lang DJ5, Inoue S6, Honer WG7


    Reduced hippocampal volume in schizophrenia is a well-replicated finding. New imaging techniques allow delineation of hippocampal subfield volumes. Studies including predominantly chronic patients demonstrate differences between subfields in sensitivity to illness, and in associations with clinical features. We carried out a cross-sectional and longitudinal study of first episode, sub-chronic, and chronic patients, using an imaging strategy that allows for the assessment of multiple hippocampal subfields.


    Hippocampal subfield volumes were measured in 34 patients with schizophrenia (19 first episode, 6 sub-chronic, 9 chronic) and 15 healthy comparison participants. A subset of 10 first episode and 12 healthy participants were rescanned after six months.


    Total left hippocampal volume was smaller in sub-chronic (p = 0.04, effect size 1.12) and chronic (p = 0.009, effect size 1.42) patients compared with healthy volunteers. The CA2-3 subfield volume of chronic patients was significantly decreased (p = 0.009, effect size 1.42) compared to healthy volunteers. The CA4-DG volume was significantly reduced in all three patient groups compared to healthy group (all p smaller than 0.005). The two affected subfield volumes were inversely correlated with severity of negative symptoms (p smaller than 0.05). There was a small, but statistically significant decline in left CA4-DG volume over the first six months of illness (p = 0.01).


    Imaging strategies defining the subfields of the hippocampus may be informative in linking symptoms and structural abnormalities, and in understanding more about progression during the early phases of illness in schizophrenia.

    adaicher1 • Feb 11, 2015 5:00 AM

    pivalde, tau pathology is involves as well and the Tau protective drug Davunetide demonstrated stat sig impact on functional capacity, also with some stat sig biomarker imaging.
    There is a lot of data out there indicating metal dyshomeostasis as being part of the problem.
    "Copper and zinc are regarded as neurotransmitters and are in high concentrations in brain hippocampus. As a result elevated copper and depressed zinc have been associated with hyperactivity, attention deficit disorders, behavior disorders, and depression. Also, many of those labeled with autism and paranoid schizophrenia have elevated blood copper levels in addition to other biochemical imbalances."
    If it is indeed copper and zinc, then PBT2 could be an option.
    And Autism from an old US study
    Conclusion: The absence of Cu and Zn homeostasis and severe Zn deficiency are suggestive of a metallothionein (MT) disorder. MT functions include neuronal development, detoxification of heavy metals, and immune response. Many classic symptoms of autism may be explained by a MT defect in infancy including G.I. tract problems, heightened sensitivity to toxic metals, and abnormal behaviors. These data suggest that an inborn error of MT functioning may be a fundamental cause of autism.
    If metal homeostasis drugs are safe, an so far it looks like they are, MPACs have the potential to be used alone or in combination over many conditions.

    kadaicher1 • Feb 11, 2015 5:04 AM

    Note they identify depressed zinc, which is exactly where PBT2 gets its tau protection from. With no plaques to pry zinc from maybe it would need to be used with a zinc drug like the one Ashley Bush was working with.
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