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      Associação entre deficiência de zinco e declínio cognitivo em idosos da comunidade Translated title: Association between zinc deficiency and cognitive decline in community-dwelling older adults

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          Abstract

          Resumo Estudo transversal avaliou a associação entre deficiência de zinco sérico e declínio cognitivo em 591 idosos da comunidade residentes nos municípios de Campinas, Limeira e Piracicaba-SP. A cognição foi avaliada pelo Instrumento de Triagem de Habilidades Cognitivas-CASI-S considerando declínio pontuação <23 em idosos de 60-69 anos e <20 em idosos ≥70 anos. Considerou-se deficiência de zinco sérico valor de <70 µg/dL para mulheres e 74 µg/dL para homens. Entre os domínios cognitivos, idosos com deficiência de zinco tiveram pontuação média significativamente menor no teste de memória (p=0,018). A prevalência da deficiência de zinco foi de 3,9%, e de 9,4% de declínio cognitivo, sendo significativamente maior em idosos com deficiência de zinco do que os que não tinham (26,1% e 8,8%, respectivamente). Em análise de regressão logística múltipla ajustada, os fatores que permaneceram associados ao declínio cognitivo foram deficiência de zinco (OR=3,80; IC95%=1,30-11,12), baixa escolaridade (OR=3,12; IC95%=1,49-6,50), não ter companheiro (OR=1,88; IC95%=1,04-3,42), risco de desnutrição (OR=3,98; IC95%=2,36-6,71), e histórico de acidente vascular encefálico (OR=2,70; IC95%=1,04-6,98). A deficiência de zinco foi associada ao declínio cognitivo em idosos. Ações na atenção básica de saúde são necessárias para prevenir a deficiência deste nutriente.

          Translated abstract

          Abstract This is a cross-sectional study evaluating the association between zinc deficiency and cognitive decline in 591 community-dwelling older adults living in the cities of Campinas, Limeira, and Piracicaba-SP. Cognitive status was evaluated using the Cognitive Abilities Screening Instrument-CASI-S, considering a decline for scores <23 for those aged 60-69 and <20 for those aged ≥70 years. Among the evaluated cognitive domains, older adults with zinc deficiency had significantly lower mean scores on the memory test (p=0.018). For zinc deficiency, values below 70 µg/dL were considered for women and 74 µg/dL for men. The prevalence of zinc deficiency was 3.9%, and cognitive deficit was 9.4%, being significantly higher in those with zinc deficiency compared with those with normal serum zinc concentrations. In adjusted multiple logistic regression analysis, the factors that remained associated with cognitive decline were zinc deficiency (OR=3.80; 95%CI=1.30-11.12), low schooling level (OR=3.12; 95%CI=1.49-6.50), lack of a partner (OR=1.88; 95%CI=1.04-3.42), risk of malnutrition (OR=3.98; 95%CI=2.36-6.71), and a history of encephalic vascular accident (OR=2.70; 95%CI=1.04-6.98). Zinc deficiency was associated with the presence of cognitive decline in older adults. Actions in primary health care are necessary to prevent the deficiency of this nutrient.

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          Most cited references46

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          The neurobiology of zinc in health and disease.

          The use of zinc in medicinal skin cream was mentioned in Egyptian papyri from 2000 BC (for example, the Smith Papyrus), and zinc has apparently been used fairly steadily throughout Roman and modern times (for example, as the American lotion named for its zinc ore, 'Calamine'). It is, therefore, somewhat ironic that zinc is a relatively late addition to the pantheon of signal ions in biology and medicine. However, the number of biological functions, health implications and pharmacological targets that are emerging for zinc indicate that it might turn out to be 'the calcium of the twenty-first century'.
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            Post-stroke dementia – a comprehensive review

            Post-stroke dementia (PSD) or post-stroke cognitive impairment (PSCI) may affect up to one third of stroke survivors. Various definitions of PSCI and PSD have been described. We propose PSD as a label for any dementia following stroke in temporal relation. Various tools are available to screen and assess cognition, with few PSD-specific instruments. Choice will depend on purpose of assessment, with differing instruments needed for brief screening (e.g., Montreal Cognitive Assessment) or diagnostic formulation (e.g., NINDS VCI battery). A comprehensive evaluation should include assessment of pre-stroke cognition (e.g., using Informant Questionnaire for Cognitive Decline in the Elderly), mood (e.g., using Hospital Anxiety and Depression Scale), and functional consequences of cognitive impairments (e.g., using modified Rankin Scale). A large number of biomarkers for PSD, including indicators for genetic polymorphisms, biomarkers in the cerebrospinal fluid and in the serum, inflammatory mediators, and peripheral microRNA profiles have been proposed. Currently, no specific biomarkers have been proven to robustly discriminate vulnerable patients (‘at risk brains’) from those with better prognosis or to discriminate Alzheimer’s disease dementia from PSD. Further, neuroimaging is an important diagnostic tool in PSD. The role of computerized tomography is limited to demonstrating type and location of the underlying primary lesion and indicating atrophy and severe white matter changes. Magnetic resonance imaging is the key neuroimaging modality and has high sensitivity and specificity for detecting pathological changes, including small vessel disease. Advanced multi-modal imaging includes diffusion tensor imaging for fiber tracking, by which changes in networks can be detected. Quantitative imaging of cerebral blood flow and metabolism by positron emission tomography can differentiate between vascular dementia and degenerative dementia and show the interaction between vascular and metabolic changes. Additionally, inflammatory changes after ischemia in the brain can be detected, which may play a role together with amyloid deposition in the development of PSD. Prevention of PSD can be achieved by prevention of stroke. As treatment strategies to inhibit the development and mitigate the course of PSD, lowering of blood pressure, statins, neuroprotective drugs, and anti-inflammatory agents have all been studied without convincing evidence of efficacy. Lifestyle interventions, physical activity, and cognitive training have been recently tested, but large controlled trials are still missing.
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              The relationship between obesity and cognitive health and decline

              The relationship between obesity and cognitive impairment is important given the globally ageing population in whom cognitive decline and neurodegenerative disorders will carry grave individual, societal and financial burdens. This review examines the evidence for the link between obesity and cognitive function in terms of both the immediate effects on cognitive performance, and effects on the trajectory of cognitive ageing and likelihood of dementia. In mid-life, there is a strong association between obesity and impaired cognitive function. Anthropometric measures of obesity are also associated with reduced neural integrity (e.g. grey and white matter atrophy). Increasing age coupled with the negative metabolic consequences of obesity (e.g. type 2 diabetes mellitus) are likely to significantly contribute to cognitive decline and incidence of dementia. Stress is identified as a potential risk factor promoting abdominal obesity and contributing to impaired cognitive function. However, the potentially protective effects of obesity against cognitive decline in older age require further examination. Finally, surgical and whole diet interventions, which address obesity may improve cognitive capacity and confer some protection against later cognitive decline. In conclusion, obesity and its comorbidities are associated with impaired cognitive performance, accelerated cognitive decline and neurodegenerative pathologies such as dementia in later life. Interventions targeting mid-life obesity may prove beneficial in reducing the cognitive risks associated with obesity.
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                Author and article information

                Journal
                csc
                Ciência & Saúde Coletiva
                Ciênc. saúde coletiva
                ABRASCO - Associação Brasileira de Saúde Coletiva (Rio de Janeiro, RJ, Brazil )
                1413-8123
                1678-4561
                2022
                : 27
                : 7
                : 2805-2816
                Affiliations
                [4] Limeira orgnameUniversidade Estadual de Campinas orgdiv1Faculdade de Ciências Aplicadas orgdiv2Laboratório de Distúrbios do Metabolismo Brazil
                [2] Campinas São Paulo orgnameUniversidade Estadual de Campinas orgdiv1Faculdade de Ciências Médicas orgdiv2Departamento de Gerontologia Brazil
                [1] Limeira orgnameUniversidade Estadual de Campinas orgdiv1Faculdade de Ciências Aplicadas orgdiv2Laboratório de Epidemiologia Nutricional Brazil mafmarchetti@ 123456gmail.com
                [3] Alfenas Minas Gerais orgnameUniversidade Federal de Alfenas orgdiv1Faculdade de Nutrição orgdiv2Departamento de Saúde Coletiva Brazil
                Article
                S1413-81232022000702805 S1413-8123(22)02700702805
                10.1590/1413-81232022277.19932021
                35730848
                f161217a-cdc0-4d45-b249-60e140c4b821

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

                History
                : 08 July 2021
                : 16 February 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 46, Pages: 12
                Product

                SciELO Public Health

                Categories
                Temas Livres

                Zinco,Cognição,Idosos,Zinc,Cognition,Older adults
                Zinco, Cognição, Idosos, Zinc, Cognition, Older adults

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