18 research outputs found

    BIN1 knockdown has no effect on APP processing.

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    <p>SH-SY5Y cells were transfected with either siRNA against BIN1 (+) or non-targeting control siRNA (-). Representative immunoblots of cell lysates (BIN1 and APP) and conditioned media samples (sAPPα and sAPPβ) (A). Fluorescence microscopy images of BIN1 (green) and DAPI staining (blue) (C). Densitometric analysis of BIN1 (B), APP (D) and sAPPα and sAPPβ (E) relative to total protein. ELISA analysis of Aβ40 and Aβ42 in conditioned media (F). Data represent mean ± S.D., n=3, *p<0.05, Independent T-test.</p

    CNTN5 does not correlate with Aβ load, soluble Aβ or insoluble Aβ.

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    <p>Relative CNTN5 protein levels were plotted against Aβ load (A), soluble Aβ (B) and insoluble Aβ (C) for each subject in the cohort (n = 48. Control, filled circles; AD, empty circles). CNTN5 levels did not correlate with Aβ load, soluble Aβ or insoluble Aβ levels as determined by Spearman's rank correlation coefficient (r<sub>s</sub>).</p

    Effect of BIN1 overexpression on APP processing.

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    <p>SH-SY5Y cells were transfected with either BIN1 cDNA (+) or empty vector (-). Representative immunoblots of cell lysates (BIN1 and APP) and conditioned media samples (sAPPα and sAPPβ) (A). Densitometric analysis of APP (B) and sAPPα and sAPPβ (C) relative to total protein. ELISA analysis of Aβ40 and Aβ42 in conditioned media (D). Data represent mean ± S.D., n=3, *p<0.05, Independent T-test. </p

    PrP<sup>C</sup> inversely correlates with BACE1 activity, Aβ load, soluble and insoluble Aβ and Braak stage.

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    <p>Relative PrP<sup>C</sup> protein levels were plotted against BACE1 activity (A), Aβ load (B), soluble Aβ (C), insoluble Aβ (D) and Braak stage (E) for each subject in the cohort (n = 48. Control, filled circles; AD, empty circles). PrP<sup>C</sup> significantly inversely correlates with BACE1 activity, Aβ load, soluble Aβ, insoluble Aβ and Braak stage as determined by Spearman's rank correlation coefficient (r<sub>s</sub>).</p

    BIN1 does not correlate with soluble or insoluble Aβ, Aβ load or Tau pathology in sporadic AD samples.

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    <p>Relative BIN1 protein levels of sporadic AD samples were plotted against soluble Aβ (A), insoluble Aβ (B), Aβ load (C) and tau pathology (D) for each subject in the cohort (n = 24). BIN1 does not correlate with soluble Aβ, insoluble Aβ, Aβ load and tau pathology as determined by Spearman’s rank correlation coefficient (r<sub>s</sub>). </p

    PrP<sup>C</sup>, but not CNTN5, is decreased in sporadic AD.

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    <p>Representative immunoblots of PrP<sup>C</sup> and actin in temporal cortex samples from sporadic AD patients compared to age-matched controls (A) with densitometric analysis relative to actin levels represented in a grouped scatter plot (B). Representative immunoblots of CNTN5 relative to actin (C) with densitometry analysis (D). Line represents mean, *p<0.05, n = 24 per group.</p

    BIN1 is decreased in sporadic AD, but not in familial AD and does not correlate with age.

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    <p>Representative immunoblot of BIN1 in temporal cortex samples from sporadic AD patients compared to age-matched controls (A) with densitometric analysis of all bands relative to total protein represented in a group scatter plot, n = 24 per group, Mann Whitney U (B) and data omitting the 3 outlying control samples n = 21 control, n = 24 AD, Mann Whitney U (inset B). Line represents mean, error bar represents SD, *p<0.05. Immunoblot of BIN1 in hippocampal samples from familial AD patients compared to age-matched controls (C) with densitometric analysis relative to total protein represented in a group scatter plot (D). Line represents mean, error bar represents SD, n = 6 per group, Indepentent T-test. Immunoblot of BIN1 in hippocampal samples of a series of non-dementia brains covering a wide spectrum of ages (E) with densitometric analysis relative to total protein, n = 16 (F). BIN1 does not correlate with age as determined by Spearman’s rank correlation coefficient (r<sub>s</sub>).</p
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