The Safety and Efficacy of Neramexane in Patients With Moderate to Severe Alzheimer's Disease
Memory loss and difficulties with thinking associated with Alzheimer's disease may be due to chronic release of a brain chemical called glutamate. Glutamate helps transmit messages between nerve cells through interaction with a certain type of receptor (N-methyl-D-aspartate, NMDA) on the cell. Neramexane is a new drug that blocks the effects of excessive glutamate at the receptor (NMDA receptor antagonist).
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double-Blind, Primary Purpose: Treatment
Pivotal Research Centers
Results (where available)
- Source: http://clinicaltrials.gov/show/NCT00090116
- Information obtained from ClinicalTrials.gov on July 15, 2010
Primary: - To assess the influence of acidified urinary pH on the renal excretion of Neramexane Secondary: - To assess the influence of acidified urinary pH on the renal exc...
Primary Objectives: • Assess the effects of poly-specific cytochrome P450 and drug-transporter induction by repeated dose Rifampicin (600 mg/day) co-administration on the single-dose ...
Primary: To assess the effects of CYP2B6 inhibition by repeated dose Clopidogrel (75 mg/day) co-administration on the single-dose pharmacokinetics of Neramexane Secondary: T...
Primary: - To assess the effects of ascending repeated-doses of oral [p.o.] neramexane at therapeutic and supra-therapeutic steady-state doses on cardiac repolarisation (QT/QTc ...
The purpose of this study is to investigate the long-term safety, tolerability and efficacy of neramexane mesylate in the treatment of congenital idiopathic nystagmus (CIN). In addition, a...
Risk factors for developing Alzheimer disease include hypercholesterolemia, hypertension, obesity, and diabetes. Due to lack of effective treatments for Alzheimer disease (AD), primary prevention beco...
There is little knowledge of the long-term course of Alzheimer disease (AD) in light of current pharmacological and nonpharmacological interventions provided in a "real-life" setting.
In vivo imaging of brain β-amyloid, a hallmark of Alzheimer disease, may assist in the clinical assessment of suspected Alzheimer disease.
Medical and Biotech [MESH] Definitions
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 precursor to the AMYLOID BETA-PROTEIN (beta/A4). Alterations in the expression of the amyloid beta-protein precursor (ABPP) gene, located on chromosome 21, plays a role in the development of the neuropathology common to both ALZHEIMER DISEASE and DOWN SYNDROME. ABPP is associated with the extensive extracellular matrix secreted by neuronal cells. Upon cleavage, this precursor produces three proteins of varying amino acid lengths: 695, 751, and 770. The beta/A4 (695 amino acids) or beta-amyloid protein is the principal component of the extracellular amyloid in senile plaques found in ALZHEIMER DISEASE; DOWN SYNDROME and, to a limited extent, in normal aging.
A chromosome disorder associated either with an extra chromosome 21 or an effective trisomy for chromosome 21. Clinical manifestations include hypotonia, short stature, brachycephaly, upslanting palpebral fissures, epicanthus, Brushfield spots on the iris, protruding tongue, small ears, short, broad hands, fifth finger clinodactyly, Simian crease, and moderate to severe MENTAL RETARDATION. Cardiac and gastrointestinal malformations, a marked increase in the incidence of LEUKEMIA, and the early onset of ALZHEIMER DISEASE are also associated with this condition. Pathologic features include the development of NEUROFIBRILLARY TANGLES in neurons and the deposition of AMYLOID BETA-PROTEIN, similar to the pathology of ALZHEIMER DISEASE. (Menkes, Textbook of Child Neurology, 5th ed, p213)