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Articles by Paul B. Rosenberg
Total Records ( 2 ) for Paul B. Rosenberg
  Lea T. Drye , Zahinoor Ismail , Anton P. Porsteinsson , Paul B. Rosenberg , Daniel Weintraub , Daniel Weintraub , Daniel Weintraub , Constantine Frangakis , Peter V. Rabins , Cynthia A. Munro , Curtis L. Meinert , D.P. Devanand , Jerome Yesavage , Jacobo E. Mintzer , Lon S. Schneider , Bruce G. Pollock and Constantine G. Lyketsos
  Background Agitation is one of the most common neuropsychiatric symptoms of Alzheimer‘s disease (AD), and is associated with serious adverse consequences for patients and caregivers. Evidence-supported treatment options for agitation are limited. The citalopram for agitation in Alzheimer‘s disease (CitAD) study was designed to evaluate the potential of citalopram to ameliorate these symptoms. Methods CitAD is a randomized, double-masked, placebo-controlled multicenter clinical trial, with two parallel treatment groups assigned in a 1:1 ratio and randomization stratified by clinical center. The study included eight recruiting clinical centers, a chair‘s office, and a coordinating center located in university settings in the United States and Canada. A total of 200 individuals having probable AD with clinically significant agitation and without major depression were recruited for this study. Patients were randomized to receive citalopram (target dose of 30 mg/d) or matching placebo. Caregivers of patients in both treatment groups received a structured psychosocial therapy. Agitation was compared between treatment groups using the NeuroBehavioral Rating Scale and the AD Cooperative Study- Clinical Global Impression of Change, which are the primary outcomes. Functional performance, cognition, caregiver distress, and rates of adverse and serious adverse events were also measured. Conclusion The authors believe the design elements in CitAD are important features to be included in trials assessing the safety and efficacy of psychotropic medications for clinically significant agitation in AD.
  Jonathan A. Stiber , Zhu -Shan Zhang , Jarrett Burch , Jerry P. Eu , Sarah Zhang , George A. Truskey , Malini Seth , Naohiro Yamaguchi , Gerhard Meissner , Ripal Shah , Paul F. Worley , R. Sanders Williams and Paul B. Rosenberg
  Transient receptor potential (TRP) channels are nonselective cation channels, several of which are expressed in striated muscle. Because the scaffolding protein Homer 1 has been implicated in TRP channel regulation, we hypothesized that Homer proteins play a significant role in skeletal muscle function. Mice lacking Homer 1 exhibited a myopathy characterized by decreased muscle fiber cross-sectional area and decreased skeletal muscle force generation. Homer 1 knockout myotubes displayed increased basal current density and spontaneous cation influx. This spontaneous cation influx in Homer 1 knockout myotubes was blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRPC1. Moreover, diminished Homer 1 expression in mouse models of Duchenne`s muscular dystrophy suggests that loss of Homer 1 scaffolding of TRP channels may contribute to the increased stretch-activated channel activity observed in mdx myofibers. These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP channels and regulates mechanotransduction in skeletal muscle.
 
 
 
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