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      Dietary fish oil increases catalase activity in patients with probable Alzheimer's disease Translated title: El aceite de pescado en la dieta aumenta la actividad de la catalasa en pacientes con probable enfermedad de Alzheimer

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          Abstract

          Abstract Background: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the presence of neuritic plaques and neurofibrillary tangles that finally result in synaptic and neuronal loss. Oxidative stress accompanies pathological changes in AD. Objective: to assess the efficacy of dietary omega 3 polyunsaturated fatty acids supplementation on the levels of proteins oxidation, hydroperoxides and enzymatic activities of catalase and superoxide dismutase in AD patients. Methods: clinical, controlled, randomized, double-blind trial. Patients consumed fish oil or placebo for one year. Oxidative stress markers were assessed in plasma using spectrophotometric methods. Results: carbonyl groups in proteins and hydroperoxides in plasma have similar values in both treatment groups at the beginning of the study. At six and 12 months of treatment, these values decreased significantly in the fish oil group, while in the placebo group no changes were observed in both oxidative stress markers. Catalase activity increased significantly at six and twelve months after treatment in patients treated with fish oil. While the superoxide dismutase activity was not modified in both study groups. Conclusions: patients who consume omega 3 polyunsaturated fatty acids at a stable dose of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) show decreased oxidation of proteins and lipids in plasma. In addition, an increase in catalase activity was detected. Thus, the presented data warrants further studies evaluating the antioxidant effect of omega 3 polyunsaturated fatty acids.

          Translated abstract

          Resumen Antecedentes: la enfermedad de Alzheimer (EA) es un trastorno neurodegenerativo caracterizado por la presencia de placas neuríticas y ovillos neurofibrilares que finalmente resultan en pérdida sináptica y neuronal. El estrés oxidativo acompaña los cambios patológicos en la EA. Objetivo: evaluar la eficacia de la suplementación dietética con ácidos grasos poliinsaturados omega 3 sobre los niveles de oxidación de proteínas, hidroperóxidos y actividades enzimáticas de catalasa y superóxido dismutasa en pacientes con EA. Métodos: ensayo clínico, controlado, aleatorizado, doble ciego. Los pacientes consumieron aceite de pescado o placebo durante un año. Los marcadores de estrés oxidativo se evaluaron en plasma mediante métodos espectrofotométricos. Resultados: los grupos carbonilo en proteínas e hidroperóxidos en plasma tuvieron valores similares en ambos grupos de tratamiento al inicio del estudio. A los seis y 12 meses de tratamiento estos valores disminuyeron significativamente en el grupo de aceite de pescado, mientras que en el grupo placebo no se observaron cambios en ambos marcadores. La actividad de catalasa aumentó significativamente a los seis y doce meses después del tratamiento en pacientes tratados con aceite de pescado; sin embargo, la actividad superóxido dismutasa no se modificó en ambos grupos de estudio. Conclusiones: los pacientes que consumieron los ácidos grasos poliinsaturados omega 3 a una dosis estable de ácido docosahexaenoico (DHA) y ácido eicosapentaenoico (EPA) muestran una oxidación reducida de proteínas y lípidos en plasma. Además, se detectó un aumento en la actividad de la catalasa. Por tanto, los datos presentados justifican más estudios que evalúen el efecto antioxidante de dichos ácidos grasos.

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          Clinical diagnosis of Alzheimer's disease: Report of the NINCDS-ADRDA Work Group* under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease

          Neurology, 34(7), 939-939
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            The neuropathological diagnosis of Alzheimer’s disease

            Alzheimer’s disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. The cardinal pathological features of the disease have been known for more than one hundred years, and today the presence of these amyloid plaques and neurofibrillary tangles are still required for a pathological diagnosis. Alzheimer’s disease is the most common cause of dementia globally. There remain no effective treatment options for the great majority of patients, and the primary causes of the disease are unknown except in a small number of familial cases driven by genetic mutations. Confounding efforts to develop effective diagnostic tools and disease-modifying therapies is the realization that Alzheimer’s disease is a mixed proteinopathy (amyloid and tau) frequently associated with other age-related processes such as cerebrovascular disease and Lewy body disease. Defining the relationships between and interdependence of various co-pathologies remains an active area of investigation. This review outlines etiologically-linked pathologic features of Alzheimer’s disease, as well as those that are inevitable findings of uncertain significance, such as granulovacuolar degeneration and Hirano bodies. Other disease processes that are frequent, but not inevitable, are also discussed, including pathologic processes that can clinically mimic Alzheimer’s disease. These include cerebrovascular disease, Lewy body disease, TDP-43 proteinopathies and argyrophilic grain disease. The purpose of this review is to provide an overview of Alzheimer’s disease pathology, its defining pathologic substrates and the related pathologies that can affect diagnosis and treatment. Electronic supplementary material The online version of this article (10.1186/s13024-019-0333-5) contains supplementary material, which is available to authorized users.
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              Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease

              Alzheimer’s disease (AD) is a devastating neurodegenerative disorder without a cure. Most AD cases are sporadic where age represents the greatest risk factor. Lack of understanding of the disease mechanism hinders the development of efficacious therapeutic approaches. The loss of synapses in the affected brain regions correlates best with cognitive impairment in AD patients and has been considered as the early mechanism that precedes neuronal loss. Oxidative stress has been recognized as a contributing factor in aging and in the progression of multiple neurodegenerative diseases including AD. Increased production of reactive oxygen species (ROS) associated with age- and disease-dependent loss of mitochondrial function, altered metal homeostasis, and reduced antioxidant defense directly affect synaptic activity and neurotransmission in neurons leading to cognitive dysfunction. In addition, molecular targets affected by ROS include nuclear and mitochondrial DNA, lipids, proteins, calcium homeostasis, mitochondrial dynamics and function, cellular architecture, receptor trafficking and endocytosis, and energy homeostasis. Abnormal cellular metabolism in turn could affect the production and accumulation of amyloid-β (Aβ) and hyperphosphorylated Tau protein, which independently could exacerbate mitochondrial dysfunction and ROS production, thereby contributing to a vicious cycle. While mounting evidence implicates ROS in the AD etiology, clinical trials with antioxidant therapies have not produced consistent results. In this review, we will discuss the role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease.
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                Author and article information

                Journal
                nh
                Nutrición Hospitalaria
                Nutr. Hosp.
                Grupo Arán (Madrid, Madrid, Spain )
                0212-1611
                1699-5198
                December 2022
                : 39
                : 6
                : 1364-1368
                Affiliations
                [3] Guadalajara orgnameUniversidad de Guadalajara orgdiv1Centro universitario de Ciencias Exactas e Ingeniería orgdiv2Department of Chemistry Mexico
                [4] Guadalajara Jalisco orgnameInstituto Mexicano del Seguro Social (IMSS) orgdiv1Centro de Investigación Biomédica de Occidente (CIBO) orgdiv2Department of Neurology. High Speciality Medical unit Mexico
                [2] Guadalajara orgnameUniversidad de Guadalajara orgdiv1Centro universitario de Ciencias de la Salud orgdiv2Department of Philosophical and Methodological Disciplines and Molecular Biology in Medicine HC Mexico
                [5] Guadalajara Jalisco orgnameKurago Biotek Mexico
                [1] Guadalajara Jalisco orgnameInstituto Mexicano del Seguro Social (IMSS) orgdiv1Centro de Investigación Biomédica de Occidente (CIBO) orgdiv2Neurosciences Division Mexico
                Article
                S0212-16112022001000020 S0212-1611(22)03900600020
                10.20960/nh.04153
                36327127
                5e1c24f2-829f-4c40-a622-c884117dd331

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

                History
                : 21 August 2022
                : 08 April 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 28, Pages: 5
                Product

                SciELO Spain

                Categories
                Original Papers

                Enfermedad de Alzheimer,Protein carbonyls,Catalase,Omega 3 polyunsaturated fatty acids,Oxidative stress,Alzheimer's disease,Carbonilos proteicos,Catalasa,Ácidos grasos poliinsaturados omega 3,Estrés oxidativo

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