scholarly journals P3-020: AXS-05, A NOVEL ORAL NMDA RECEPTOR ANTAGONIST WITH MULTI-MODAL ACTIVITY IN CLINICAL DEVELOPMENT FOR AGITATION ASSOCIATED WITH ALZHEIMER'S DISEASE

2019 ◽  
Vol 15 ◽  
pp. P932-P932
Author(s):  
Cedric O'Gorman ◽  
Amanda Jones ◽  
Herriot Tabuteau
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist ◽  
Clinical Development

scholarly journals STRATEGIES FOR MANAGEMENT OF ALZHEIMER’S DISEASE: A REVIEW

2020 ◽  
Vol 11 (12) ◽  
pp. 7-16
Author(s):  
Ishu Sharma ◽  
Ankit Kumar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Mechanism Of Action ◽  
Cholinesterase Inhibitors ◽  
Nmda Receptor Antagonist ◽  
Review Article ◽  
Way Of Life ◽  
Day By Day

Alzheimer’s is the most widely recognized reason for dementia discovered by Alois Alzheimer’s in 1906. Severity of Alzheimer’s disease is increments with age and mostly after 65 years. It is a progressive neurodegenerative disease that damage memory and intellectual capacities. It affects 34 million people worldwide and as time goes, the pervasiveness of Alzheimer’s disease continues to increase and as indicated by WHO it can reaches to 95 million by 2050. Manifestation of Alzheimer’s incorporates cognitive decline that changes day by day way of life, trouble in finishing everyday errands, disarray with time or spot, misguide thinking. Most preferred drugs used for Alzheimer’s are cholinesterase inhibitors like Donepezil, rivastigmine, Galantamine, Tacrine, NMDA receptor antagonist like memantine. The purpose of this review article is to provide a brief introduction, potential causes, symptoms and mechanism of action of Alzheimer’s disease. This review article likewise accentuation on utilization of therapeutic plants and isolated compounds for preventing and reducing the symptoms of Alzheimer’s disease.

Current Treatments for Alzheimer’s Disease

2017 ◽  
Author(s):  
Mary Sano ◽  
Judith Neugroschil
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Clinical Trials ◽  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Drug Administration ◽  
Acetylcholinesterase Inhibitors ◽  
Nmda Receptor Antagonist ◽  
Metabolic Risk ◽  
The Us

Five medications representing two classes of drugs have been approved by the US Food and Drug Administration for the treatment of Alzheimer’s disease since 1994. There have been no new approved agents since 2003, although hundreds of clinical trials are in progress. This chapter reviews the pharmacology underlying the currently approved treatments, acetylcholinesterase inhibitors and the NMDA receptor antagonist memantine, and the data supporting their efficacy. Other approaches currently in use or being developed are also reviewed, including the use of hormones, agents that modify cardiovascular and metabolic risk, as well as a number of vitamin supplements and nutritional approaches.

scholarly journals Treatment of Moderate to Severe Alzheimer's Disease: Rationale and Trial Design

2007 ◽  
Vol 34 (S1) ◽  
pp. S103-S108 ◽  
Author(s):  
Nathan Herrmann
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nmda Receptor ◽  
Caregiver Burden ◽  
Trial Design ◽  
Cholinesterase Inhibitors ◽  
Nmda Receptor Antagonist ◽  
Disease Modifying ◽  
Disease Modifying Agents ◽  
Complete Dependence

Moderate to severe Alzheimer's disease (AD) is characterized by increasing cognitive, functional, and behavioural dysfunction that results in increased caregiver burden and, eventually, complete dependence. Despite its significance as a societal health problem, there are few treatment trials of cognitive enhancers or disease modifying agents for this stage of illness. Studies suggest the cholinesterase inhibitors, especially donepezil, may provide benefit. Several studies provide support for the use of the NMDA receptor antagonist memantine as monotherapy or added to a cholinesterase inhibitor for moderate to severe AD. While there are no published guidelines for the treatment of moderate to severe AD, these studies do provide guidance for recommendations for study design and outcome measures. Such studies are urgently needed.

scholarly journals The pathological hallmarks of Alzheimer’s disease derive from compensatory responses to NMDA receptor insufficiency

2018 ◽  
Author(s):  
Selina Sohre ◽  
Bernd Moosmann
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nmda Receptor ◽  
Cortical Neurons ◽  
Amyloid Β ◽  
Nmda Receptor Antagonist ◽  
Amyloid Β Peptide ◽  
App Processing ◽  
Mk 801 ◽  
Compensatory Responses

AbstractAlzheimer’s disease is characterized by intracellular aggregates of hyperphosphorylated tau protein and extracellular plaques of amyloid β peptide, a product of APP processing. The origin of these pathological hallmarks has remained elusive. Here, we have tested the idea that both alterations, at the onset of the disease, may constitute compensatory responses to the same causative and initial trigger, namely NMDA receptor insufficiency. Treatment of rat cortical neurons with the specific NMDA receptor antagonist AP5 within 4 h caused a significant increase in tau phosphorylation at the AT8 and S404 epitopes as well as an increase in APP expression and Aβ 40 secretion. Single intraperitoneal injections of the NMDA receptor open channel blocker MK-801 into wild-type mice reproduced all of these changes in a brain region-specific fashion either at latency 4 h or 24 h. Subchronic treatment with MK-801 for 6 weeks induced AT8, S404 and S396 immunoreactivity selectively in female mice. We conclude that the pivotal pathological alterations in Alzheimer’s disease represent runaway physiological responses to persistently insufficient excitatory neurotransmission. In view of the evidence for excitatory insufficiency in trisomy 21 patients, PS1 mutation carriers and ApoE4 carriers, our data suggest a common pathomechanism behind familial, sporadic, and risk allele-triggered Alzheimer’s disease. The potential of this mechanism to reconcile previous conflicting observations is discussed.

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