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      Patogenia y tratamientos actuales de la enfermedad de Alzheimer Translated title: Pathogenesis and current treatment of Alzheimer's disease

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          El Alzheimer es una enfermedad neurodegenerativa que se manifiesta como deterioro cognitivo y trastornos conductuales. En Cuba, junto a la demencia, ocupa el lugar número 6 en el cuadro de principales causas de muerte. No hay tratamiento eficaz para detener la progresión del Alzheimer. Sin embargo, algunas terapias detienen o ralentizan temporalmente el deterioro cognitivo, funcional y conductual de la enfermedad. En el trabajo se presenta una revisión actualizada a partir de la base de datos MEDLINE (2008-2013) sobre los mecanismos patológicos y los medicamentos usados en el tratamiento de los pacientes con la referida afección.

          Translated abstract

          Alzheimer disease is a neurodegenerative illness that manifests as cognitive deterioration and behavioral disorders. It holds the 6th place, like dementia, in the list of main causes of death in Cuba. There is no effective treatment to stop progression of Alzheimer's disease. However, some therapies manage to halt or to slow at least temporarily the cognitive, functional and behavioral deterioration of the disease. This paper presented an updated review on the pathological mechanisms and the drugs used in the treatment of Alzheimer patients, using MEDLINE database.

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          The diagnosis of dementia due to Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease

          Guy M McKhann, David S. Knopman, Howard Chertkow … (2011)
          The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of revising the 1984 criteria for Alzheimer's disease (AD) dementia. The workgroup sought to ensure that the revised criteria would be flexible enough to be used by both general healthcare providers without access to neuropsychological testing, advanced imaging, and cerebrospinal fluid measures, and specialized investigators involved in research or in clinical trial studies who would have these tools available. We present criteria for all-cause dementia and for AD dementia. We retained the general framework of probable AD dementia from the 1984 criteria. On the basis of the past 27 years of experience, we made several changes in the clinical criteria for the diagnosis. We also retained the term possible AD dementia, but redefined it in a manner more focused than before. Biomarker evidence was also integrated into the diagnostic formulations for probable and possible AD dementia for use in research settings. The core clinical criteria for AD dementia will continue to be the cornerstone of the diagnosis in clinical practice, but biomarker evidence is expected to enhance the pathophysiological specificity of the diagnosis of AD dementia. Much work lies ahead for validating the biomarker diagnosis of AD dementia. Copyright © 2011. Published by Elsevier Inc.
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            Introduction to the recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease.

            Clifford R. Jack, Marilyn S Albert, David S. Knopman … (2011)
            Criteria for the clinical diagnosis of Alzheimer's disease (AD) were established in 1984. A broad consensus now exists that these criteria should be revised to incorporate state-of-the-art scientific knowledge. The National Institute on Aging (NIA) and the Alzheimer's Association sponsored a series of advisory round table meetings in 2009 whose purpose was to establish a process for revising diagnostic and research criteria for AD. The recommendation from these advisory meetings was that three separate work groups should be formed with each assigned the task of formulating diagnostic criteria for one phase of the disease: the dementia phase; the symptomatic, pre-dementia phase; and the asymptomatic, preclinical phase of AD. Two notable differences from the AD criteria published in 1984 are incorporation of biomarkers of the underlying disease state and formalization of different stages of disease in the diagnostic criteria. There was a broad consensus within all three workgroups that much additional work is needed to validate the application of biomarkers for diagnostic purposes. In the revised NIA-Alzheimer's Association criteria, a semantic and conceptual distinction is made between AD pathophysiological processes and clinically observable syndromes that result, whereas this distinction was blurred in the 1984 criteria. The new criteria for AD are presented in three documents. The core clinical criteria of the recommendations regarding AD dementia and MCI due to AD are intended to guide diagnosis in the clinical setting. However, the recommendations of the preclinical AD workgroup are intended purely for research purposes. Copyright © 2011 The Alzheimer's Association. All rights reserved.
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              Neurobiological markers of exercise-related brain plasticity in older adults.

              Brandt Pence, Laura Chaddock-Heyman, Edward McAuley … (2013)
              The current study examined how a randomized one-year aerobic exercise program for healthy older adults would affect serum levels of brain-derived neurotrophic factor (BDNF), insulin-like growth factor type 1 (IGF-1), and vascular endothelial growth factor (VEGF) - putative markers of exercise-induced benefits on brain function. The study also examined whether (a) change in the concentration of these growth factors was associated with alterations in functional connectivity following exercise, and (b) the extent to which pre-intervention growth factor levels were associated with training-related changes in functional connectivity. In 65 participants (mean age=66.4), we found that although there were no group-level changes in growth factors as a function of the intervention, increased temporal lobe connectivity between the bilateral parahippocampus and the bilateral middle temporal gyrus was associated with increased BDNF, IGF-1, and VEGF for an aerobic walking group but not for a non-aerobic control group, and greater pre-intervention VEGF was associated with greater training-related increases in this functional connection. Results are consistent with animal models of exercise and the brain, but are the first to show in humans that exercise-induced increases in temporal lobe functional connectivity are associated with changes in growth factors and may be augmented by greater baseline VEGF. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (publisher-id): far
                Title: Revista Cubana de Farmacia
                Abbreviated Title: Rev Cubana Farm
                Publisher: Editorial Ciencias Médicas (Ciudad de la Habana, , Cuba )
                ISSN (Print): 0034-7515
                ISSN (Electronic): 1561-2988
                Publication date (Print and electronic): September 2014
                Volume: 48
                Issue: 3
                Pages: 508-518
                Affiliations
                [02] Ancona orgnameMedical Center Beauty Benefit srl Italy
                [01] La Habana orgnamePoliclínico Vedado. Plaza de la Revolución Cuba
                Article
                Publisher ID: S0034-75152014000300016 Publisher ID: S0034-7515(14)04800316
                SO-VID: 4c332568-cff9-43a5-a66b-dcedef9657e4
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                Date received : 22 July 2014
                Date accepted : 15 August 2014
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 41, Pages: 11
                Product

                SciELO Cuba

                Self URI: Texto completo solamente en formato PDF (ES)
                Categories
                Subject: ARTICULOS DE REVISIÓN

                Keywords: placas beta-amiloide,deterioro cognitivo,demencia senil,Alzheimer,demencia,dementia,senile dementia,cognitive deterioration,beta-amyloid plaques
                Data availability:
                Keywords: placas beta-amiloide, deterioro cognitivo, demencia senil, Alzheimer, demencia, dementia, senile dementia, cognitive deterioration, beta-amyloid plaques

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