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Articles by Anton P. Porsteinsson
Total Records ( 2 ) for Anton P. Porsteinsson
  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.
  Martin Farlow , Steven E. Arnold , Christopher H. van Dyck , Paul S. Aisen , B. Joy Snider , Anton P. Porsteinsson , Stuart Friedrich , Robert A. Dean , Celedon Gonzales , Gopalan Sethuraman , Ronald B. DeMattos , Richard Mohs , Steven M. Paul and Eric R. Siemers
  Objectives To assess the safety, tolerability, pharmacokinetics, and pharmacodynamics of 12 weekly infusions of solanezumab, an anti-β-amyloid (Aβ) antibody, in patients with mild-to-moderate Alzheimer‘s disease. Cognitive measures were also obtained. Methods In this phase 2, randomized, double-blind, placebo-controlled clinical trial, 52 patients with Alzheimer‘s disease received placebo or antibody (100 mg every 4 weeks, 100 mg weekly, 400 mg every 4 weeks, or 400 mg weekly) for 12 weeks. Safety and biomarker evaluations continued until 1 year after randomization. Both magnetic resonance imaging and cerebrospinal fluid (CSF) examinations were conducted at baseline and after the active treatment period. The Aβ concentrations were measured in plasma and CSF, and the Alzheimer‘s Disease Assessment Scale–cognitive portion was administered. Results Clinical laboratory values, CSF cell counts, and magnetic resonance imaging scans were unchanged by treatment, and no adverse events could be clearly related to antibody administration. Total (bound to antibody and unbound) Aβ1–40 and Aβ1–42 in plasma increased in a dose-dependent manner. Antibody treatment similarly increased total Aβ1–40 and Aβ1–42 in CSF. For patients taking 400 mg weekly, antibody treatment decreased unbound Aβ1–40 in CSF (P < .01), but increased unbound Aβ1–42 in CSF in a dose-dependent manner. The Alzheimer‘s Disease Assessment Scale–cognitive portion was unchanged after the 12-week antibody administration. Conclusions Antibody administration was well tolerated with doses up to 400 mg weekly. The dose-dependent increase in unbound CSF Aβ1–42 suggests that this antibody may shift Aβ equilibria sufficiently to mobilize Aβ1–42 from amyloid plaques.
 
 
 
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