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Articles
by
Anton P. Porsteinsson |
Total Records (
2 ) for
Anton P. Porsteinsson |
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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
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Background
Agitation is one of the most common neuropsychiatric symptoms of Alzheimers 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 Alzheimers 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 chairs 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. |
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Martin Farlow
,
Steven E. Arnold
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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
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Steven M. Paul
and
Eric R. Siemers
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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 Alzheimers disease. Cognitive measures were also obtained.
Methods
In this phase 2, randomized, double-blind, placebo-controlled clinical trial, 52 patients with Alzheimers 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 Alzheimers Disease Assessment Scalecognitive 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) Aβ140 and Aβ142 in plasma increased in a dose-dependent manner. Antibody treatment similarly increased total Aβ140 and Aβ142 in CSF. For patients taking 400 mg weekly, antibody treatment decreased unbound Aβ140 in CSF (P < .01), but increased unbound Aβ142 in CSF in a dose-dependent manner. The Alzheimers Disease Assessment Scalecognitive 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 Aβ142 suggests that this antibody may shift Aβ equilibria sufficiently to mobilize Aβ142 from amyloid plaques. |
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