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Genomics of schizophrenia and pharmacogenomics of antipsychotic drugs

Open Journal of Psychiatry 2013年第1期3卷 46-139页

作者： Ramón Cacabelos Pablo Cacabelos Gjumrakch Aliev EuroEspes biomedical research Center Institute for CNS Disorders and Genomic Medicine EuroEspes Chair of Biotechnology and Genomics Camilo José Cela University Corunna Spain EuroEspes biomedical research Center Institute for CNS Disorders and Genomic Medicine EuroEspes Chair of Biotechnology and Genomics Camilo José Cela University Corunna Spain&Gally International Biomedical Research Consulting LLC San Antonio USA

Antipsychotic drugs are the neuroleptics currently used in the treatment of schizophrenia (SCZ) and psychotic disorders. SCZ has a heritability estimated at 70% - 90%;and pharmacogenomics accounts for 60% - 90% variability in the pharmacokinetics and pharmacodynamics of psychotropic drugs. Personalized therapeutics based on individual genomic profiles in SCZ entails the characterization of 5 types of gene clusters and their related metabolomic profiles: 1) genes associated with disease pathogenesis;2) genes associated with the mechanism of action of drugs;3) genes associated with drug metabolism (phase I and II reactions);4) genes associated with drug transporters;and 5) pleiotropic genes involved in multifaceted cascades and metabolic reactions. Genetic studies in SCZ have revealed the presence of chromosome anomalies, copy number variants, multiple single-nucleotide polymorphisms of susceptibility distributed across the human genome, aberrant single-nucleotide polymorphisms in microRNA genes, mitochondrial DNA mutations, and epigenetic phenomena. Pharmacogenetic studies of psychotropic drug response have focused on determining the relationship between variation in specific candidate genes and the positive and adverse effects of drug treatment. Approximately 18% of neuroleptics are major substrates of CYP1A2 enzymes, 40% of CYP2D6, and 23% of CYP3A4. About 10% - 20% of Western populations are defective in genes of the CYP superfamily. Only 26% of Southern Europeans are pure extensive metabolizers for the trigenic cluster integrated by the CYP2D6 + CYP2C19 + CYP2C9 genes. Efficacy and safety issues in the pharmacological treatment of SCZ are directly linked to genetic clusters involved in the pharmacogenomics of antipsychotic drugs and also to environmental factors. Consequently, the incorporation of pharmacogenomic procedures both to drugs under development and drugs on the market would help to optimize therapeutics in SCZ and other central nervous system disorders

关键词： Genomics Antipsychotic Drugs Schizophrenia

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Human photosynthesis, the ultimate answer to the long term mystery of Kleiber’s law or E = M<sup>3/4</sup>: Implication in the context of gerontology and neurodegenerative diseases

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Open Journal of Psychiatry 2013年第4期3卷 408-421页

作者： Gjumrakch Aliev Arturo Solís-Herrera Yi Li Yury G. Kaminsky Nikolay N. Yakhno Vladimir N. Nikolenko Andrey A. Zamyatnin Jr. Valery V. Benberin Sergey O. Bachurin Department of Anatomy First Moscow State Medical University Moscow Russian Federation Department of Neurological Disorders First Moscow State Medical University Moscow Russian Federation Institute of Physiologically Active Compounds Russian Academy of Sciences Chernogolovka Russian Federation Medical Center of the Administration of the President of the Republic of Kazakhstan Astana Kazakhstan Russian Academy of Sciences Institute of Theoretical and Experimental Biophysics Pushchino Russian Federation “gally” international biomedical research consulting llc San Antonio USA Human Photosynthesis Study Center Pulgas Pandas Sur México Institute of Molecular Medicine First Moscow State Medical University Moscow Russian Federation Department of Human Sciences Texas A&M University-Kingsville Kingsville USA

Kleiber’s Law or E = M3/4 is a mathematical expression known since 1932 that outlines the relationship between mass (biomass) and the use of energy. It is compelling because it supports a long standing observation that larger animals appear to use energy more efficiently than smaller ones. For example, an elephant’s weight is 200,000 times of a mouse, but uses only about 10,000 fold energy;thus a cat, having a mass of about 100 times of a mouse, only spends roughly 33 fold energy. In other words, the bigger you are, the less energy per gram of tissue you actually need to stay alive. Many facts pertaining to animal size call for a rational explanation. This paper takes into account that the fascinating relationship between mass and energy use for any living thing is governed strictly by a mathematical universal formula across all living species, operating in the tiniest of bacteria to the biggest of whales and sequoia tress. For the first time, we report a capacity for the mammal eukaryotic cell to split, break or dissociate water molecules through melanin. Even though E = M3/4 was discovered eight decades ago, no proper satisfactory explanation exists. Nevertheless, our multiyear detailed study on the “Human Photosynthesis” or first found in the human retina and later in all eukaryotic cells, may finally unravel this mystery, namely, the bigger you are the more surface area you have to absorb electromagnetic radiation and the more potential exists to use that electromagnetic radiation spectra to perform work. We propose a future application of this theory in the context of human diseases, especially age-related disorders, such as retinopathy, cerebrovascular and Alzheimer disease and these implications may not only foster a better understanding of the pathobiology of these devastating diseases but also develop much more effective therapies in the foreseeable future.

关键词： Human Photosynthesis Kleiber’s Law Geriatrics Gerontology Cardio- and Cerebrovascular Diseases Neurodegeneration Alzheimer Disease Retinopathy

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