GABAergic signaling abnormalities in a novel CLU mutation Alzheimer's disease mouse model.The CLU rs11136000C mutation (CLUC) is the third most common risk factor for Alzheimer's disease (AD).  However, the mechanism by which CLUC leads to abnormal GABAergic signaling in AD is unclear.  To address this question, this study establishes the first chimeric mouse model of CLUC AD.  Examination of grafted CLUC medial ganglionic eminence progenitors (CLUC hiMGEs) revealed increased GAD65/67 and a high frequency of spontaneous releasing events.  CLUC hiMGEs also impaired cognition in chimeric mice and caused AD-related pathologies.  Taken together, these findings shed light on the pathogenesis of CLUC AD using a novel humanized animal model and suggest sphingolipid signaling over-activation as a potential mechanism of GABAergic signaling disorder.
CLU
GABAergic signaling abnormalities in a novel CLU mutation Alzheimer's disease mouse model.The CLU rs11136000C mutation (CLUC) is the third most common risk factor for Alzheimer's disease (AD).  However, the mechanism by which CLUC leads to abnormal GABAergic signaling in AD is unclear.  To address this question, this study establishes the first chimeric mouse model of CLUC AD.  Examination of grafted CLUC medial ganglionic eminence progenitors (CLUC hiMGEs) revealed increased GAD65/67 and a high frequency of spontaneous releasing events.  CLUC hiMGEs also impaired cognition in chimeric mice and caused AD-related pathologies.  Taken together, these findings shed light on the pathogenesis of CLUC AD using a novel humanized animal model and suggest sphingolipid signaling over-activation as a potential mechanism of GABAergic signaling disorder.
CLU
GABAergic signaling abnormalities in a novel CLU mutation Alzheimer's disease mouse model.The CLU rs11136000C mutation (CLUC) is the third most common risk factor for Alzheimer's disease (AD).  However, the mechanism by which CLUC leads to abnormal GABAergic signaling in AD is unclear.  To address this question, this study establishes the first chimeric mouse model of CLUC AD.  Examination of grafted CLUC medial ganglionic eminence progenitors (CLUC hiMGEs) revealed increased GAD65/67 and a high frequency of spontaneous releasing events.  CLUC hiMGEs also impaired cognition in chimeric mice and caused AD-related pathologies.  Taken together, these findings shed light on the pathogenesis of CLUC AD using a novel humanized animal model and suggest sphingolipid signaling over-activation as a potential mechanism of GABAergic signaling disorder.
CLU
GABAergic signaling abnormalities in a novel CLU mutation Alzheimer's disease mouse model.The CLU rs11136000C mutation (CLUC) is the third most common risk factor for Alzheimer's disease (AD).  However, the mechanism by which CLUC leads to abnormal GABAergic signaling in AD is unclear.  To address this question, this study establishes the first chimeric mouse model of CLUC AD.  Examination of grafted CLUC medial ganglionic eminence progenitors (CLUC hiMGEs) revealed increased GAD65/67 and a high frequency of spontaneous releasing events.  CLUC hiMGEs also impaired cognition in chimeric mice and caused AD-related pathologies.  Taken together, these findings shed light on the pathogenesis of CLUC AD using a novel humanized animal model and suggest sphingolipid signaling over-activation as a potential mechanism of GABAergic signaling disorder.
CLU
GABAergic signaling abnormalities in a novel CLU mutation Alzheimer's disease mouse model.The CLU rs11136000C mutation (CLUC) is the third most common risk factor for Alzheimer's disease (AD).  However, the mechanism by which CLUC leads to abnormal GABAergic signaling in AD is unclear.  To address this question, this study establishes the first chimeric mouse model of CLUC AD.  Examination of grafted CLUC medial ganglionic eminence progenitors (CLUC hiMGEs) revealed increased GAD65/67 and a high frequency of spontaneous releasing events.  CLUC hiMGEs also impaired cognition in chimeric mice and caused AD-related pathologies.  Taken together, these findings shed light on the pathogenesis of CLUC AD using a novel humanized animal model and suggest sphingolipid signaling over-activation as a potential mechanism of GABAergic signaling disorder.
CLU