[Back to Contents Page]

 

 

 

Current Pharmaceutical Design, Volume 8, No. 2, 2002

 

Contents

 

Central Nervous System Agents

Executive  Editors: Joseph P. Yevich / David W. Smith

 

A Review of Molecular Modeling Approaches to Pharmacophore Models and Structure-Activity Relationships of Ion Channel Modulators in CNS Pp-99-110

Y. Li and W. E. Harte

[Abstract]

 

Quantitative Structure-Activity Relationship Studies on Cholecystokinin Antagonists Pp-111-124

Satya P. Gupta

[Abstract]

 

Design and Study of Piracetam-like Nootropics,Controversial Members of the Problematic Class of Cognition-Enhancing Drugs Pp-125-138

Fulvio Gualtieri, Dina Manetti, Maria Novella Romanelli and Carla Ghelardini

[Abstract]

 

The Potential Utility of 5-HT1A Receptor Antagonists in the Treatment of Cognitive Dysfunction Associated with Alzheimer’s Disease Pp-139-145

L.E. Schechter, L.A. Dawson and J.A. Harder

[Abstract]

 

Analysis of Overall Gene Expression Induced by Amphetamine and Phencyclidine: Novel Targets for the Treatment of Drug Psychosis and Schizophrenia Pp-147-153

Chihiro Ito

[Abstract]

 


Abstracts

 

[Back to top] A Review of Molecular Modeling Approaches to Pharmacophore Models and Structure-Activity Relationships of Ion Channel Modulators in CNS 

Y. Li and W. E. Harte

 

Through pharmacophore models and providing quantitative analysis of structure-activity relationships (QSAR), molecular modeling techniques can be useful tools to study the interactions of ion channels and their modulators. The present review focuses on molecular modeling approaches that defined pharmacophore models of ion channel modulators in the CNS. The commonality and subtlety of the pharmacophore models of various ion channel modulators are discussed which can be used as a framework for the design of ion channel modulators.

 

[Back to top]  Quantitative Structure-Activity Relationship Studies on Cholecystokinin Antagonists

Satya P. Gupta

 

A review is presented on quantitative structure-activity relationship (QSAR) studies on cholecystokinin antagonists. Cholecystokinin (CCK) is a gastrointestinal peptide hormone closely related chemically to gastrin. However, its receptors are found in both peripheral and central nervous systems. Those present in peripheral system have been termed as CCK-A receptors and those present in central nervous system as CCK-B receptors. QSAR studies verify that CCK-B receptors are closely related structurally to gastrin recetors. QSAR studies have been reported on different classes of CCK antagonists, e.g., benzodiazepine derivatives, amino acid derivatives, quinazolinones, and peptides and pseudopeptide analogs. These QSAR studies unravel the mechanisms of interactions of each category of antagonists with the CCK receptors. In the case of benzodiazepines, the hydrophobic interactions and hydrogen bondings are found to be the most important binding force, while in the case of quinazolinones, only the hydrogen bonding is found to be important. The hydrophobic as well as the dispersion interactions are shown to be important for the binding of glutamic acid analogs and steric factors appear to govern the activity of peptides and pseudopeptide analogs.

 

[Back to top]  Design and Study of Piracetam-like Nootropics, Controversial Members of the Problematic Class of Cognition-Enhancing Drugs

Fulvio Gualtieri, Dina Manetti, Maria Novella Romanelli and Carla Ghelardini

 

Cognition enhancers are drugs able to facilitate attentional abilities and acquisition, storage and retrieval of information, and to attenuate the impairment of cognitive functions associated with head traumas, stroke, age and age-related  pathologies. Development of  cognition  enhancers is still a difficult task because of complexity of the brain functions, poor predictivity of animal tests and lengthy and expensive clinical trials. After the early serendipitous discovery of first generation cognition enhancers, current research is based on a variety of working hypotheses, derived from the progress of knowledge in the neurobiopathology of cognitive processes.

 

Among other classes of drugs, piracetam-like cognition enhancers (nootropics) have never reached general acceptance, in spite of their excellent tolerability and safety. In the present review, after a general discussion of the problems connected with the design and development of cognition enhancers, the class is examined in more detail. Reasons for the problems encountered by nootropics, compounds therapeutically available and those in development, their structure activity relationships and mechanisms of action are discussed. Recent developments which hopefully will lead to a revival of the class are reviewed.

 

[Back to top]  The Potential Utility of 5-HT1A Receptor Antagonists in the Treatment of Cognitive Dysfunction Associated with Alzheimer’s Disease

L.E. Schechter, L.A. Dawson and J.A. Harder

 

The 5-HT1Areceptor has been extensively studied over the last two decades. There is a plethora of information describing its anatomical, physiological and biochemical roles in the brain. In addition, the development of selective pharmacological tools coupled with our understanding of psychiatric pathology has lead to multiple hypotheses for the therapeutic utility of 5-HT1A agents and in particular 5-HT1A receptor antagonists. Over the last decade it has been suggested that 5-HT1A receptor antagonists may have therapeutic utility in such diseases as depression, anxiety, drug and nicotine withdrawal as well as schizophrenia. However, a very compelling rationale has been developed for the therapeutic potential of 5-HT1A receptor antagonists in Alzheimer's disease and potentially other diseases with associated cognitive dysfunction. Receptor blockade by a 5-HT1A receptor antagonist appears to enhance activation and signaling through heterosynaptic neuronal circuits known to be involved in cognitive processes and, as such, represents a novel therapeutic approach to the treatment of cognitive deficits associated with Alzheimer's disease and potentially other disorders with underlying cognitive dysfunction.

 

[Back to top] Analysis of Overall Gene Expression Induced byAmphetamine and Phencyclidine: Novel Targets for the Treatment of Drug Psychosis and Schizophrenia

Chihiro Ito

 

Although the etiology of drug psychosis or schizophrenia is still unknown, molecular and biochemical researches have recently made significant advances in the search for the candidate genes of these disorders. Among such studies are animal models of drug psychosis or schizophrenia such as amphetamine-induced behavioral sensitization or phencyclidine-treated animals. In this review, it is suggested that amphetamine or phencyclidine change the gene expressions related to not only neurotransmistter systems such as dopamine or glutamic acid, transcription factors, cell proliferation, apoptosis, cell adhesion, but also the synapse. These alterable gene expressions may lead to the discovery of candidate genes of drug psychosis or schizophrenia and thus to novel antipsychotics.