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Rivastigmine Monotherapy and Combination Therapy With Memantine in Patients With Moderately Severe Alzheimer's Disease Who Failed to Benefit From Previous Cholinesterase Inhibitor Treatment

2014-08-27 03:48:23 | BioPortfolio

Summary

This is a prospective, multicenter, open-label study. Following screening and baseline assessments, eligible patients will be switched to rivastigmine and will enter the 16 week run-in rivastigmine treatment phase. After completion of assessments at the end of the run-in phase, patients who were not sufficiently stabilized on rivastigmine alone will receive add-on memantine to their rivastigmine treatment; patients who were stabilized on rivastigmine alone will have completed and be discontinued from the study.

Study Design

Allocation: Non-Randomized, Control: Uncontrolled, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Treatment

Conditions

Alzheimer's Disease

Intervention

Rivastigmine, memantine

Location

Département de Gérontologie Clinique
Limoges
Cedex
France
87042

Status

Completed

Source

Novartis

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:48:23-0400

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A carbamate-derived reversible CHOLINESTERASE INHIBITOR that is selective for the CENTRAL NERVOUS SYSTEM and is used for the treatment of DEMENTIA in ALZHEIMER DISEASE and PARKINSON DISEASE.

Abnormal structures located chiefly in distal dendrites and, along with NEUROFIBRILLARY TANGLES and SENILE PLAQUES, constitute the three morphological hallmarks of ALZHEIMER DISEASE. Neuropil threads are made up of straight and paired helical filaments which consist of abnormally phosphorylated microtubule-associated tau proteins. It has been suggested that the threads have a major role in the cognitive impairment seen in Alzheimer disease.

Vaccines or candidate vaccines used to prevent or treat ALZHEIMER DISEASE.

A progressive form of dementia characterized by the global loss of language abilities and initial preservation of other cognitive functions. Fluent and nonfluent subtypes have been described. Eventually a pattern of global cognitive dysfunction, similar to ALZHEIMER DISEASE, emerges. Pathologically, there are no Alzheimer or PICK DISEASE like changes, however, spongiform changes of cortical layers II and III are present in the TEMPORAL LOBE and FRONTAL LOBE. (From Brain 1998 Jan;121(Pt 1):115-26)

A biochemical phenomenon in which misfolded proteins aggregate either intra- or extracellularly. Triggered by factors such as MUTATION, POST-TRANSLATIONAL MODIFICATIONS, and environmental stress, it is generally associated with ALZHEIMER DISEASE; PARKINSON DISEASE; HUNTINGTON DISEASE; and TYPE 2 DIABETES MELLITUS.

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