Browsing by Author "Zhu, Timothy"

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    Author Correction: Salt-dependent Blood Pressure in Human Aldosterone Synthase-Transgenic Mice
    (Springer Nature, 2018-10-25) Gu, Huiying; Ma, Zhizhong; Wang, Jian; Zhu, Timothy; Du, Nicole; Shatara, Adam; Yi, Xin; Kowala, Mark C.; Du, Yansheng; Neurology, School of Medicine
    A correction has been published and is appended to both the HTML and PDF versions of this paper. The error has not been fixed in the paper.
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    IVIG Delays Onset in a Mouse Model of Gerstmann-Sträussler-Scheinker Disease
    (Springer Nature, 2019-04) Gu, Huiying; Kirchhein, Yvonne; Zhu, Timothy; Zhao, Gang; Peng, Hongjun; Du, Eileen; Liu, Junyi; Mastrianni, James A.; Farlow, Martin R.; Dodel, Richard; Du, Yansheng; Neurology, School of Medicine
    Our previous studies showed that intravenous immunoglobulin (IVIG) contained anti-Aβ autoantibodies that might be able to treat Alzheimer's disease (AD). Recently, we identified and characterized naturally occurring autoantibodies against PrP from IVIG. Although autoantibodies in IVIG blocked PrP fibril formation and PrP neurotoxicity in vitro, it remained unknown whether IVIG could reduce amyloid plaque pathology in vivo and be used to effectively treat animals with prion diseases. In this study, we used Gerstmann-Sträussler-Scheinker (GSS)-Tg (PrP-A116V) transgenic mice to test IVIG efficacy since amyloid plaque formation played an important role in GSS pathogenesis. Here, we provided strong evidence that demonstrates how IVIG could significantly delay disease onset, elongate survival, and improve clinical phenotype in Tg (PrP-A116V) mice. Additionally, in treated animals, IVIG could markedly inhibit PrP amyloid plaque formation and attenuate neuronal apoptosis at the age of 120 days in mice. Our results indicate that IVIG may be a potential, effective therapeutic treatment for GSS and other prion diseases.
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    Salt-dependent Blood Pressure in Human Aldosterone Synthase-Transgenic Mice
    (Springer Nature, 2017-03-28) Gu, Huiying; Ma, Zhizhong; Wang, Jian; Zhu, Timothy; Du, Nicole; Shatara, Adam; Yi, Xin; Kowala, Mark C.; Du, Yansheng; Department of Neurology, IU School of Medicine
    Hypertension is one of the most important, preventable causes of premature morbidity and mortality in the developed world. Aldosterone is a major mineralocorticoid hormone that plays a key role in the regulation of blood pressure and is implicated in the pathogenesis of hypertension and heart failure. Aldosterone synthase (AS, cytochrome P450 11B2, cyp11B2) is the sole enzyme responsible for the production of aldosterone in humans. To determine the effects of increased expression of human aldosterone synthase (hAS) on blood pressure (BP), we established transgenic mice carrying the hAS gene (cyp11B2). We showed that hAS overexpression increased levels of aldosterone in hAS+/− mice. On high salt diet (HS), BPs of hAS+/− mice were significantly increased compared with WT mice. Fadrozole (an inhibitor of aldosterone synthase) treatment significantly reduced BPs of hAS+/− mice on HS. This is the first time overexpression of AS in a transgenic mouse line has shown an ability to induce HP. Specifically inhibiting AS activity in these mice is a promising therapy for reducing hypertension. This hAS transgenic mouse model is therefore an ideal animal model for hypertension therapy studies.