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Lopez-Munoz F.,Camilo Jose Cela University | Lopez-Munoz F.,University of Alcala | Lopez-Munoz F.,Hospital 12 Of Octubre Research Institute I12 | Shen W.W.,Taipei Medical University | And 8 more authors.
Journal of Experimental and Clinical Medicine (Taiwan) | Year: 2014

In this review, we analyzed the status and changes in the research on second-generation (atypical) antipsychotic drugs in the Asia-Pacific region (i.e., Japan, South Korea, Taiwan, Hong Kong, Singapore, and Australia). We also performed a bibliometric study of the literature in this region on atypical antipsychotic drugs (e.g., clozapine, risperidone, olanzapine, ziprasidone, quetiapine, sertindole, aripiprazole, paliperidone, amisulpride, zotepine, asenapine, iloperidone, lurasidone, perospirone, and blonanserin). We applied bibliometric indicators of production and dispersion (i.e., Price's law on the increase of scientific literature and Bradford's law, respectively). We also calculated the participation index of different countries. The data were also correlated with relevant social and health data from the Asia-Pacific region (e.g., the per capita gross domestic product and total per capita expenditure on health and gross domestic expenditure on research and development). All data are discussed together. We also analyzed the different aspects among the six countries in the region. © 2014. Source

Cacabelos R.,Camilo Jose Cela University | Cacabelos R.,Institute for Medical Science and Genomic Medicine | Torrellas C.,Institute for Medical Science and Genomic Medicine | Lopez-Munoz F.,Camilo Jose Cela University | And 2 more authors.
Journal of Experimental and Clinical Medicine (Taiwan) | Year: 2014

Alzheimer's disease (AD) is a polygenic/complex disorder in which genomic, epigenomic, and environmental factors are involved. Epigenetic factors have emerged as important mediators of aging, neurodegeneration, and brain disorders. Epigenomic changes underlying the phenotypic expression of AD, represented by deposits of extracellular Aβ aggregates in senile plaques, intracellular neurofibrillary tangles, neuronal loss, dendritic desarborization, and neurochemical alterations are candidate targets for therapeutic intervention. Changes in DNA methylation, histone modifications, chromatin remodeling, and noncoding RNA dysregulation can affect AD-related gene expression, leading to the multistep process of premature neurodegeneration. Epigenetic modifications are reversible and can be potentially targeted by pharmacological and dietary interventions. © 2014 Elsevier Taiwan LLC. Source

Cacabelos R.,Camilo Jose Cela University | Cacabelos R.,Institute for CNS Disorders and Genomic Medicine | Torrellas C.,Institute for CNS Disorders and Genomic Medicine | Fernandez-Novoa L.,Institute for CNS Disorders and Genomic Medicine | And 2 more authors.
Mediators of Inflammation | Year: 2016

Neuroimmune dysregulation is a common phenomenon in different forms of central nervous system (CNS) disorders. Cross-links between central and peripheral immune mechanisms appear to be disrupted as reflected by a series of immune markers (CD3, CD4, CD7, HLA-DR, CD25, CD28, and CD56) which show variability in brain disorders such as anxiety, depression, psychosis, stroke, Alzheimer's disease, Parkinson's disease, attention-deficit hyperactivity disorder, migraine, epilepsy, vascular dementia, mental retardation, cerebrovascular encephalopathy, multiple sclerosis, brain tumors, cranial nerve neuropathies, mental retardation, and posttraumatic brain injury. Histamine (HA) is a pleiotropic monoamine involved in several neurophysiological functions, neuroimmune regulation, and CNS pathogenesis. Changes in brain HA show an age- and sex-related pattern, and alterations in brain HA levels are present in different CNS regions of patients with Alzheimer's disease (AD). Brain HA in neuronal and nonneuronal compartments plays a dual role (neurotrophic versus neurotoxic) in a tissue-specific manner. Pathogenic mechanisms associated with neuroimmune dysregulation in AD involve HA, interleukin-1β, and TNF-α, whose aberrant expression contributes to neuroinflammation as an aggravating factor for neurodegeneration and premature neuronal death. © 2016 Ramón Cacabelos et al. Source

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