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1.
Hipertens. riesgo vasc ; 37(3): 125-132, jul.-sept. 2020. graf, tab
Artigo em Espanhol | IBECS | ID: ibc-193521

RESUMO

La hipertensión arterial es considerada el principal factor de riesgo vascular modificable que causa daño en forma silente en los vasos del cerebro. Esta injuria vascular cerebral podría ser el núcleo común que justifique los síntomas cognitivos (deterioro cognitivo, demencia y enfermedad de Alzheimer) y conductuales (depresión de inicio tardío) del daño de órgano blanco mediado por la hipertensión arterial. El conocimiento incompleto sobre los complejos vínculos fisiopatológicos que relacionan la hipertensión arterial con los cambios cognitivo-conductuales soslaya la participación del cerebro como órgano blanco subestimando el riesgo cardio y cerebrovascular. La convergencia de deterioro cognitivo, depresión e hipertensión arterial en adultos mayores, advierte sobre la necesidad de una evaluación integral que permita planificar el tratamiento, mejorar pronóstico y contribuir a la disminución del riesgo de demencia y su incidencia


Arterial hypertension is considered the main modifiable vascular risk factor that causes silent damage to brain vessels. This vascular brain injury could be the common nucleus that justifies the cognitive (cognitive impairment, dementia and Alzheimer's disease) and behavioural symptoms (late-life depression) of target organ damage mediated-hypertension. Incomplete knowledge about the complex pathophysiology that links hypertension with cognitive-behavioural changes is overlooking brain involvement and underestimating cardio and cerebrovascular risk. The confluence of cognitive impairment, depression and arterial hypertension in elderly adults, warns of the need for a comprehensive evaluation to plan treatment, improve prognosis and contribute to reducing the risk of dementia and its incidence


Assuntos
Humanos , Hipertensão/fisiopatologia , Hipertensão/psicologia , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/psicologia , Disfunção Cognitiva/prevenção & controle , Transtornos de Início Tardio/fisiopatologia , Doença de Alzheimer/etiologia , Fatores de Risco
2.
Yakugaku Zasshi ; 140(9): 1129-1139, 2020.
Artigo em Japonês | MEDLINE | ID: mdl-32879245

RESUMO

The medical information and communication technology "Kibitan Health Net" was introduced as a part of the medical reconstruction assistance national project in Fukushima. However, its effect on the performance of the pharmacists has not yet been validated in community pharmacy. In this study, we investigated the usefulness of acquisition and utilization of precise medical information from diabetic patients using Kibitan Health Net. The subjects of this study were 18 patients having type 2 diabetes mellitus with a mean HbA1c level of 7.4±1.0 (%). We compared the HbA1c level captured by the pharmacists from the patients (total 72 times) with that updated on Kibitan Health Net (41 times correctly captured by the pharmacists). We next compared the HbA1c levels between the "group that could listen to accurate laboratory data" and the "group that could not listen to accurate laboratory data" using intergroup analysis. After factor analysis between the two groups, we demonstrated that the proportion of patients who could not precisely communicate laboratory results was significantly higher among the elderly population (p<0.05). Recent studies have reported that elderly diabetic patients have a higher risk of cognitive decline and Alzheimer-type dementia resulting in higher brain dysfunction. The utilization of Kibitan Health Net enabled the capturing of precise patient information. These data could make it possible to provide instruction for proper compliance and guidance for recuperation among the elderly diabetic patients, and prevent their cognitive decline due to poor glycemic control, as well as set future therapeutic goals and improve adherence.


Assuntos
Diabetes Mellitus/diagnóstico , Hemoglobina A Glicada/análise , Tecnologia da Informação , Farmacêuticos , Adulto , Idoso , Idoso de 80 Anos ou mais , Doença de Alzheimer/etiologia , Doença de Alzheimer/prevenção & controle , Biomarcadores/sangue , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/prevenção & controle , Complicações do Diabetes/etiologia , Complicações do Diabetes/prevenção & controle , Feminino , Humanos , Japão , Masculino , Pessoa de Meia-Idade , Cooperação do Paciente , Farmácias , Encaminhamento e Consulta , Adulto Jovem
3.
Medicine (Baltimore) ; 99(39): e22381, 2020 Sep 25.
Artigo em Inglês | MEDLINE | ID: mdl-32991458

RESUMO

INTRODUCTION: The mean age of the German population increased over the last years, which resulted in a higher prevalence of cardiovascular diseases, type 2 diabetes, cognitive impairment, sarcopenia and bone fractures. Current evidence indicates a preservation of human wellbeing in the elderly by a healthy diet, although the recommended macronutrient composition and quality remains unclear and needs further long-term investigation. In this context we investigate the effect of a specific dietary pattern on age-related disorders in a randomized controlled multi-center trial (RCT). METHODS: We assess the effect of a specific dietary pattern (NutriAct) with a high proportion of unsaturated fat, plant proteins and fibres (fat 35%-40% of total energy (%E) of which 15%E-20%E monounsaturated fatty acids (MUFA) and 10%E-15%E polyunsaturated fatty acids (PUFA), 15%E-25%E proteins, ≥30 g fibres per day and 35%E-45%E carbohydrates) on age-related impairment of health within a 36-months RCT conducted in the region of Berlin and Potsdam. 502 eligible men (n = 183) and women (n = 319), aged 50 to 80 years, with an increased risk to develop age-related diseases were randomly assigned to either an intervention group focusing on NutriAct dietary pattern or a control group focusing on usual care and dietary recommendations in accordance to the German Nutrition Society (DGE). In the intervention group, 21 nutrition counsellings as well as supplementation of rapeseed oil, oil cake and specific designed foods are used to achieve the intended NutriAct dietary pattern.The primary outcome is a composite endpoint of age-related disorders, including cardiovascular morbidity, decline of cognitive function as well as clinical features of sarcopenia. Secondary outcomes include diet-induced effects on quality of life, depression, frailty, cardiovascular function, bone density, fat distribution pattern, glucose, lipid and energy metabolism, as well as the identification of biomarkers linked with age-related disorders. DISCUSSION: The findings of this trial will provide clinically relevant information regarding dietary effects on age-related impairment of health and will contribute to the definition of the optimal macronutrient composition in the context of healthy aging in the German population.


Assuntos
Doenças Cardiovasculares/prevenção & controle , Disfunção Cognitiva/prevenção & controle , Dieta Saudável , Envelhecimento Saudável , Sarcopenia/prevenção & controle , Humanos , Estudos Multicêntricos como Assunto , Ensaios Clínicos Controlados Aleatórios como Assunto
4.
J Prev Alzheimers Dis ; 7(4): 294-298, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32920634

RESUMO

Individuals experiencing brain aging, cognitive decline, and dementia are currently confronted with several more complex challenges due to the current Sars-Cov-2 pandemic as compared to younger and cognitively healthy people. During the first six months of the pandemic, we are experiencing critical issues related to the management of mild cognitive impairment (MCI) and dementia. The evolving, highly contagious global viral spread has created a pressure test of unprecedented proportions for the existing brain health care infrastructure and related services for management, diagnosis, treatment, and prevention. Social distancing and lock-down measures are catalyzing and accelerating a technological paradigm shift, away from a traditional model of brain healthcare focused on late symptomatic disease stages and towards optimized preventive strategies to slow brain aging and increase resilience at preclinical asymptomatic stages. Digital technologies transform global healthcare for accessible equality of opportunities in order to generate better outcomes for brain aging aligned with the paradigm of preventive medicine.


Assuntos
Doença de Alzheimer/prevenção & controle , Disfunção Cognitiva/prevenção & controle , Infecções por Coronavirus , Relações Interpessoais , Pandemias , Pneumonia Viral , Isolamento Social/psicologia , Idoso , Idoso de 80 Anos ou mais , Envelhecimento , Doença de Alzheimer/psicologia , Betacoronavirus , Disfunção Cognitiva/psicologia , Progressão da Doença , Humanos , Masculino , Quarentena/psicologia , Fatores de Risco , Tecnologia
6.
Arch Dis Child Fetal Neonatal Ed ; 105(5): 466-473, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32623370

RESUMO

BACKGROUND: Progressive ventricular dilatation after intraventricular haemorrhage (IVH) in preterm infants has a very high risk of severe disability and death. Drainage, irrigation and fibrinolytic therapy (DRIFT), in a randomised controlled trial (RCT), reduced severe cognitive impairment at 2 years. OBJECTIVE: To assess if the cognitive advantage of DRIFT seen at 2 years persisted until school age. PARTICIPANTS: The RCT conducted in four centres recruited 77 preterm infants with IVH and progressive ventricular enlargement over specified measurements. Follow-up was at 10 years of age. INTERVENTION: Intraventricular injection of a fibrinolytic followed by continuous lavage, until the drainage was clear, and standard care consisting of control of expansion by lumbar punctures and if expansion persisted via a ventricular access device. PRIMARY OUTCOME: Cognitive quotient (CQ), derived from the British Ability Scales and Bayley III Scales, and survival without severe cognitive disability. RESULTS: Of the 77 children randomised, 12 died, 2 could not be traced, 10 did not respond and 1 declined at 10-year follow-up. 28 in the DRIFT group and 24 in the standard treatment group were assessed by examiners blinded to the intervention. The mean CQ score was 69.3 (SD=30.1) in the DRIFT group and 53.7 (SD=35.7) in the standard treatment group (unadjusted p=0.1; adjusted p=0.01, after adjustment for the prespecified variables sex, birth weight and IVH grade). Survival without severe cognitive disability was 66% in the DRIFT group and 35% in the standard treatment group (unadjusted p=0.019; adjusted p=0.003). CONCLUSION: DRIFT is the first intervention for posthaemorrhagic ventricular dilatation to objectively demonstrate sustained cognitive improvement. TRIAL REGISTRATION NUMBER: ISRCTN80286058.


Assuntos
Hemorragia Cerebral Intraventricular/terapia , Disfunção Cognitiva/prevenção & controle , Doenças do Prematuro/terapia , Hemorragia Cerebral Intraventricular/complicações , Criança , Comportamento Infantil , Pré-Escolar , Dilatação Patológica , Drenagem/métodos , Feminino , Seguimentos , Ventrículos do Coração/fisiopatologia , Humanos , Lactente , Recém-Nascido , Recém-Nascido Prematuro , Masculino , Punção Espinal , Irrigação Terapêutica/métodos , Terapia Trombolítica/métodos , Acuidade Visual
7.
Br J Anaesth ; 125(3): 298-307, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32624183

RESUMO

BACKGROUND: Postoperative cognitive decline (PCD) requires microglial activation. Voltage-gated Kv1.3 potassium channels are involved in microglial activation. We determined the role of Kv1.3 in PCD and the efficacy and safety of inhibiting Kv1.3 with phenoxyalkoxypsoralen-1 (PAP-1) in preventing PCD in a mouse model. METHODS: After institutional approval, we assessed whether Kv1.3-deficient mice (Kv1.3-/-) exhibited PCD, evidenced by tibial-fracture surgery-induced decline in aversive freezing behaviour, and whether PAP-1 could prevent PCD and postoperative neuroinflammation in PCD-vulnerable diet-induced obese (DIO) mice. We also evaluated whether PAP-1 altered either postoperative peripheral inflammation or tibial-fracture healing. RESULTS: Freezing behaviour was unaltered in postoperative Kv1.3-/- mice. In DIO mice, PAP-1 prevented postoperative (i) attenuation of freezing behaviour (54 [17.3]% vs 33.4 [12.7]%; P=0.03), (ii) hippocampal microglial activation by size (130 [31] pixels vs 249 [49]; P<0.001) and fluorescence intensity (12 000 [2260] vs 20 800 [5080] absorbance units; P<0.001), and (iii) hippocampal upregulation of interleukin-6 (IL-6) (14.9 [5.7] vs 25.6 [10.4] pg mg-1; P=0.011). Phenoxyalkoxypsoralen-1 neither affected surgery-induced upregulation of plasma IL-6 nor cartilage and bone components of the surgical fracture callus. CONCLUSIONS: Microglial-mediated PCD requires Kv1.3 activity, determined by genetic and pharmacological targeting approaches. Phenoxyalkoxypsoralen-1 blockade of Kv1.3 prevented surgery-induced hippocampal microglial activation and neuroinflammation in mice known to be vulnerable to PCD. Regarding perioperative safety, these beneficial effects of PAP-1 treatment occurred without impacting fracture healing. Kv1.3 blockers, currently undergoing clinical trials for other conditions, may represent an effective and safe intervention to prevent PCD.


Assuntos
Disfunção Cognitiva/prevenção & controle , Encefalite/prevenção & controle , Canal de Potássio Kv1.3/antagonistas & inibidores , Complicações Pós-Operatórias/prevenção & controle , Cicatrização/fisiologia , Animais , Modelos Animais de Doenças , Camundongos
8.
Neurology ; 95(7): e839-e846, 2020 08 18.
Artigo em Inglês | MEDLINE | ID: mdl-32669394

RESUMO

OBJECTIVE: Increasing evidence supports an association between midlife cardiovascular risk factors (CVRFs) and risk of dementia, but less is known about whether CVRFs influence cognition in midlife. We examined the relationship between CVRFs and midlife cognitive decline. METHODS: In 2,675 black and white middle-aged adults (mean age 50.2 ± 3.6 years, 57% female, 45% black), we measured CVRFs at baseline: hypertension (31%), diabetes mellitus (11%), obesity (43%), high cholesterol (9%), and current cigarette smoking (15%). We administered cognitive tests of memory, executive function, and processing speed at baseline and 5 years later. Using logistic regression, we estimated the association of CVRFs with accelerated cognitive decline (race-specific decline ≥1.5 SD from the mean change) on a composite cognitive score. RESULTS: Five percent (n = 143) of participants had accelerated cognitive decline over 5 years. Smoking, hypertension, and diabetes mellitus were associated with an increased likelihood of accelerated decline after multivariable adjustment (adjusted odds ratio [AOR] 1.65, 95% confidence interval [CI] 1.00-2.71; AOR 1.87, 95% CI 1.26-2.75; AOR 2.45, 95% CI 1.54-3.88, respectively), while obesity and high cholesterol were not associated with risk of decline. These results were similar when stratified by race. The likelihood of accelerated decline also increased with greater number of CVRFs (1-2 CVRFs: AOR 1.77, 95% CI 1.02-3.05; ≥3 CVRFs: AOR 2.94, 95% CI 1.64-5.28) and with Framingham Coronary Heart Disease Risk Score ≥10 (AOR 2.29, 95% CI 1.21-4.34). CONCLUSIONS: Midlife CVRFs, especially hypertension, diabetes mellitus, and smoking, are common and associated with accelerated cognitive decline at midlife. These results identify potential modifiable targets to prevent midlife cognitive decline and highlight the need for a life course approach to cognitive function and aging.


Assuntos
Doenças Cardiovasculares/complicações , Disfunção Cognitiva/complicações , Disfunção Cognitiva/etiologia , Hipertensão/complicações , Adulto , Idoso , Envelhecimento/fisiologia , Doenças Cardiovasculares/prevenção & controle , Cognição/fisiologia , Disfunção Cognitiva/prevenção & controle , Feminino , Humanos , Hipertensão/prevenção & controle , Masculino , Memória/fisiologia , Pessoa de Meia-Idade , Fatores de Risco
9.
PLoS One ; 15(5): e0232958, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32407347

RESUMO

INTRODUCTION: Previous evidence has shown significant effects of exercise, cognitive and dual-task training for improving cognition in healthy cohorts. The effects of these types of interventions in type 2 diabetes mellitus is unclear. The aim of this research was to systematically review evidence, and estimate the effect, of exercise, cognitive, and dual-task interventions on cognition in type 2 diabetes mellitus. METHOD: Electronic databases including PubMed, EMBASE, CINAHL, PsycINFO, SPORTDiscus, and MEDLINE were searched for ongoing and completed interventional trials investigating the effect of either an exercise, cognitive or dual-task intervention on cognition in type 2 diabetes mellitus. RESULTS: Nine trials met the inclusion criteria-one dual-task, two cognitive, and six exercise. Meta-analyses of exercise trials showed no significant effects of exercise on measures of executive function (Stroop task, SMD = -0.31, 95% CI -0.71-0.09, P = 0.13, trail making test part A SMD = 0.28, 95% CI -0.20-0.77 P = 0.25, trail making test part B SMD = -0.15, 95% CI -0.64-0.34 P = 0.54, digit symbol SMD = 0.09, 95% CI -0.39-0.57 P = 0.72), and memory (immediate memory SMD = 0.20, 95% CI -0.28-0.69, P = 0.41 and delayed memory SMD = -0.06, 95% CI -0.55-0.42, P = 0.80). A meta-analysis could not be conducted using cognitive or dual-task data, but individual trials did report a favourable effect of interventions on cognition. Risk of bias was considered moderate to high for the majority of included trials. CONCLUSIONS: Meta-analyses of exercise trials identified a small effect size (0.31), which whilst not significant warrants further investigation. Larger and more robust trials are needed that report evidence using appropriate reporting guidelines (e.g. CONSORT) to increase confidence in the validity of results. TRIAL REGISTRATION: Protocol was registered (CRD42017058526) on the International Prospective Register of Systematic Reviews (http://www.crd.york.ac.uk/PROSPERO).


Assuntos
Disfunção Cognitiva/prevenção & controle , Diabetes Mellitus Tipo 2/reabilitação , Função Executiva , Exercício Físico , Qualidade de Vida , Humanos
10.
PLoS One ; 15(5): e0232970, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32396543

RESUMO

BACKGROUND: Pooling individual participant data to enable pooled analyses is often complicated by diversity in variables across available datasets. Therefore, recoding original variables is often necessary to build a pooled dataset. We aimed to quantify how much information is lost in this process and to what extent this jeopardizes validity of analyses results. METHODS: Data were derived from a platform that was developed to pool data from three randomized controlled trials on the effect of treatment of cardiovascular risk factors on cognitive decline or dementia. We quantified loss of information using the R-squared of linear regression models with pooled variables as a function of their original variable(s). In case the R-squared was below 0.8, we additionally explored the potential impact of loss of information for future analyses. We did this second step by comparing whether the Beta coefficient of the predictor differed more than 10% when adding original or recoded variables as a confounder in a linear regression model. In a simulation we randomly sampled numbers, recoded those < = 1000 to 0 and those >1000 to 1 and varied the range of the continuous variable, the ratio of recoded zeroes to recoded ones, or both, and again extracted the R-squared from linear models to quantify information loss. RESULTS: The R-squared was below 0.8 for 8 out of 91 recoded variables. In 4 cases this had a substantial impact on the regression models, particularly when a continuous variable was recoded into a discrete variable. Our simulation showed that the least information is lost when the ratio of recoded zeroes to ones is 1:1. CONCLUSIONS: Large, pooled datasets provide great opportunities, justifying the efforts for data harmonization. Still, caution is warranted when using recoded variables which variance is explained limitedly by their original variables as this may jeopardize the validity of study results.


Assuntos
Metanálise como Assunto , Ensaios Clínicos Controlados Aleatórios como Assunto/estatística & dados numéricos , Disfunção Cognitiva/prevenção & controle , Simulação por Computador , Interpretação Estatística de Dados , Demência/prevenção & controle , Humanos , Modelos Lineares , Reprodutibilidade dos Testes , Tamanho da Amostra
11.
JAMA ; 323(19): 1934-1944, 2020 05 19.
Artigo em Inglês | MEDLINE | ID: mdl-32427305

RESUMO

Importance: The benefit of blood pressure lowering for the prevention of dementia or cognitive impairment is unclear. Objective: To determine the association of blood pressure lowering with dementia or cognitive impairment. Data Sources and Study Selection: Search of PubMed, EMBASE, and CENTRAL for randomized clinical trials published from database inception through December 31, 2019, that evaluated the association of blood pressure lowering on cognitive outcomes. The control groups consisted of either placebo, alternative antihypertensive agents, or higher blood pressure targets. Data Extraction and Synthesis: Data were screened and extracted independently by 2 authors. Random-effects meta-analysis models were used to report pooled treatment effects and CIs. Main Outcomes and Measures: The primary outcome was dementia or cognitive impairment. The secondary outcomes were cognitive decline and changes in cognitive test scores. Results: Fourteen randomized clinical trials were eligible for inclusion (96 158 participants), of which 12 reported the incidence of dementia (or composite of dementia and cognitive impairment [3 trials]) on follow-up and were included in the primary meta-analysis, 8 reported cognitive decline, and 8 reported changes in cognitive test scores. The mean (SD) age of trial participants was 69 (5.4) years and 40 617 (42.2%) were women. The mean systolic baseline blood pressure was 154 (14.9) mm Hg and the mean diastolic blood pressure was 83.3 (9.9) mm Hg. The mean duration of follow-up was 49.2 months. Blood pressure lowering with antihypertensive agents compared with control was significantly associated with a reduced risk of dementia or cognitive impairment (12 trials; 92 135 participants) (7.0% vs 7.5% of patients over a mean trial follow-up of 4.1 years; odds ratio [OR], 0.93 [95% CI, 0.88-0.98]; absolute risk reduction, 0.39% [95% CI, 0.09%-0.68%]; I2 = 0.0%) and cognitive decline (8 trials) (20.2% vs 21.1% of participants over a mean trial follow-up of 4.1 years; OR, 0.93 [95% CI, 0.88-0.99]; absolute risk reduction, 0.71% [95% CI, 0.19%-1.2%]; I2 = 36.1%). Blood pressure lowering was not significantly associated with a change in cognitive test scores. Conclusions and Relevance: In this meta-analysis of randomized clinical trials, blood pressure lowering with antihypertensive agents compared with control was significantly associated with a lower risk of incident dementia or cognitive impairment.


Assuntos
Anti-Hipertensivos/uso terapêutico , Disfunção Cognitiva/prevenção & controle , Demência/prevenção & controle , Hipertensão/tratamento farmacológico , Idoso , Pressão Sanguínea/efeitos dos fármacos , Disfunção Cognitiva/epidemiologia , Demência/epidemiologia , Feminino , Seguimentos , Humanos , Hipertensão/complicações , Masculino , Ensaios Clínicos Controlados Aleatórios como Assunto , Risco
12.
Life Sci ; 253: 117703, 2020 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-32334010

RESUMO

AIMS: Vitamin D is a well-known endocrine regulator of calcium/phosphate homeostasis and has been reported as having a wide range of activities that are potentially beneficial for human health. This study aimed to investigate the effects of pretreatment of vitamin D3 (100, 1000, and 10,000 IU/kg) against lipopolysaccharide (LPS)-induced cognitive impairment in rats. MAIN METHODS: Male Wistar rats were divided into five groups. The passive avoidance test and Morris water maze (MWM) test were conducted to evaluate the learning and memory function. Oxidative stress markers including malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), total thiol content as well as interleukin (IL)-6 were evaluated in the hippocampus tissue. KEY FINDINGS: The intraperitoneal (i.p.) injection of LPS (1 mg/kg) correlates with deficits in passive avoidance and spatial learning in the systemic inflammation model. However, pretreatment with vitamin D3 improved LPS-induced cognitive impairment. In addition, vitamin D3 decreased IL-6 and MDA levels, whereas the activities of CAT, SOD, and total thiol content in the hippocampus tissue were significantly increased. SIGNIFICANCE: In conclusion, our results suggest that vitamin D3 plays a protective role against memory dysfunction caused by LPS-induced inflammation through inhibition of oxidative stress and inflammation in the hippocampus. Vitamin D may be a promising potential therapeutic supplement for the treatment or prevention of learning and memory disorders.


Assuntos
Colecalciferol/farmacologia , Disfunção Cognitiva/prevenção & controle , Inflamação/prevenção & controle , Transtornos da Memória/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Animais , Aprendizagem da Esquiva/efeitos dos fármacos , Colecalciferol/administração & dosagem , Relação Dose-Resposta a Droga , Hipocampo/efeitos dos fármacos , Hipocampo/patologia , Lipopolissacarídeos , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Ratos , Ratos Wistar
13.
Adv Exp Med Biol ; 1260: 159-174, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32304034

RESUMO

Research in animals and humans has indicated that polyphenols can delay the age-related decline in learning, memory and neurodegenerative diseases. Among the polyphenols, berry phenolics have extensive beneficial effects because of their antioxidant and anti-inflammatory properties. Long-term consumption of grapes results in accumulation of polyphenols in the brain, which modulates cell-signalling pathways and neutralises the redox imbalance in the aging brain. Here we review the in vivo and in vitro evidence for considering grape-derived polyphenolics, the flavonoids- catechins, epicatechin, anthocyanidin, and quercetin, and non-flavonoids-gallic acid and resveratrol, as effective dietary sources to facilitate cognition in adults and lessen the decline in the old and pathogenic states, Alzheimer's and Parkinson's disease. Furthermore, a combined intervention of polyphenols along with regular physical exercise provides cognitive benefits for the aging brain and holds promising venues for preclinical and clinical studies in formulating neuro-nutraceuticals as functional foods for a healthy brain.


Assuntos
Envelhecimento/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Disfunção Cognitiva/prevenção & controle , Disfunção Cognitiva/terapia , Polifenóis/farmacologia , Polifenóis/uso terapêutico , Idoso , Envelhecimento/patologia , Animais , Antioxidantes/farmacologia , Antioxidantes/uso terapêutico , Encéfalo/patologia , Humanos
14.
Artigo em Russo | MEDLINE | ID: mdl-32323938

RESUMO

OBJECTIVE: To develop a model for the prognosis of cognitive impairment in patients with type 1 diabetes mellitus based on data from proton magnetic resonance spectroscopy. MATERIALS AND METHODS: Patients with type 1 diabetes mellitus and individuals without diabetes were examined (control group). All participants were evaluated for carbohydrate metabolism, underwent neuropsychological testing (MoCa test), proton magnetic resonance spectroscopy of the brain. Statistical processing of the results was performed using the IBM SPSS Statistics 20.0 program. The predictive model is calculated using discriminant analysis. RESULTS: Based on the data of proton magnetic resonance spectroscopy, a predictive model for the development of cognitive impairment in patients with type 1 diabetes mellitus was obtained using discriminant analysis. CONCLUSIONS: The method for the early diagnosis of cognitive impairment allows predicting the development of cognitive dysfunction in patients with type 1 diabetes in the early stages and can be used in clinical practice to assess the effectiveness of preventive therapy for cognitive impairment.


Assuntos
Disfunção Cognitiva/complicações , Disfunção Cognitiva/diagnóstico , Diabetes Mellitus Tipo 1/complicações , Diabetes Mellitus Tipo 1/psicologia , Disfunção Cognitiva/prevenção & controle , Diagnóstico Precoce , Humanos , Testes Neuropsicológicos , Prognóstico , Espectroscopia de Prótons por Ressonância Magnética
15.
Angiology ; 71(6): 498-519, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32233780

RESUMO

Growing evidence suggests that atrial fibrillation (AF), in addition to its thromboembolic risk, is a risk factor for cognitive impairment (CI) via several pathways and mechanisms, further contributing to morbidity/mortality. Prior stroke is a contributor to CI, but AF is also associated with CI independently from prior stroke. Silent brain infarctions, microemboli and microbleeds, brain atrophy, cerebral hypoperfusion from widely fluctuating ventricular rates, altered hemostatic function, vascular oxidative stress, and inflammation may all exacerbate CI, particularly in patients with persistent/permanent rather than paroxysmal AF and with increased duration/burden of the arrhythmia. Brain magnetic resonance imaging is an important screening tool in eliciting and monitoring vascular and nonvascular lesions contributing to CI. Evidence is also emerging about the role of genetics in CI development. Anticoagulation and rhythm/rate control strategies may protect against CI preventing or slowing its progression or conversion to dementia, particularly at the early stages when CI may still be a treatable condition. Importantly, AF and CI share many common risk factors. Thus, screening for these 2 conditions and searching for and managing modifiable risk factors and potentially reversible causes for both AF and CI remains an important step toward prevention or amelioration of the impact incurred by these 2 conditions.


Assuntos
Fibrilação Atrial/epidemiologia , Encéfalo/efeitos dos fármacos , Cognição , Disfunção Cognitiva/epidemiologia , Sistema de Condução Cardíaco/efeitos dos fármacos , Frequência Cardíaca , Acidente Vascular Cerebral/epidemiologia , Antiarrítmicos/uso terapêutico , Anticoagulantes/uso terapêutico , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/tratamento farmacológico , Fibrilação Atrial/fisiopatologia , Encéfalo/fisiopatologia , Tomada de Decisão Clínica , Cognição/efeitos dos fármacos , Disfunção Cognitiva/diagnóstico , Disfunção Cognitiva/fisiopatologia , Disfunção Cognitiva/prevenção & controle , Técnicas de Apoio para a Decisão , Sistema de Condução Cardíaco/fisiopatologia , Frequência Cardíaca/efeitos dos fármacos , Humanos , Prognóstico , Medição de Risco , Fatores de Risco , Acidente Vascular Cerebral/diagnóstico , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/fisiopatologia
16.
Life Sci ; 251: 117587, 2020 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-32224027

RESUMO

Diabetes mellitus (DM) is a serious public health problem and can cause long-term damage to the brain, resulting in cognitive impairment in these patients. Insulin therapy for type 1 DM (DM1) can achieve overall blood glucose control, but glycemic variations can occur during injection intervals, which may contribute to some complications. Among the additional therapies available for DM1 treatment is the implantation of insulin-producing cells (IPCs) to attenuate hyperglycemia and even reverse diabetes. Here, we studied the strategy of implanting IPCs obtained from mesenchymal stromal cells (MSCs) from adipose tissue, comparing two different IPC implant sites, subcapsular renal (SR) and subcutaneous (SC), to investigate their putative protection against hippocampal damage, induced by STZ, in a rat DM1 model. Both implants improved hyperglycemia and reduced the serum content of advanced-glycated end products in diabetic rats, but serum insulin was not observed in the SC group. The SC-implanted group demonstrated ameliorated cognitive impairment (evaluated by novel object recognition) and modulation of hippocampal astroglial reactivity (evaluated by S100B and GFAP). Using GFP+ cell implants, the survival of cells at the implant sites was confirmed, as well as their migration to the pancreas and hippocampus. The presence of undifferentiated MSCs in our IPC preparation may explain the peripheral reduction in AGEs and subsequent cognitive impairment recovery, mediated by autophagic depuration and immunomodulation at the hippocampus, respectively. Together, these data reinforce the importance of MSCs for use in neuroprotective strategies, and highlight the logistic importance of the subcutaneous route for their administration.


Assuntos
Disfunção Cognitiva/prevenção & controle , Diabetes Mellitus Experimental/terapia , Diabetes Mellitus Tipo 1/terapia , Insulina/metabolismo , Células-Tronco Mesenquimais/citologia , Tecido Adiposo/citologia , Animais , Glicemia/metabolismo , Disfunção Cognitiva/etiologia , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Tipo 1/complicações , Produtos Finais de Glicação Avançada/sangue , Hipocampo/metabolismo , Hiperglicemia/terapia , Insulina/sangue , Masculino , Pâncreas/metabolismo , Ratos , Ratos Endogâmicos WKY
17.
PLoS One ; 15(4): e0231379, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32302347

RESUMO

This randomized, double-blinded, placebo-controlled trial tested the hypothesis that 20mg of melatonin before and during the first cycle of adjuvant chemotherapy for breast cancer (ACBC) reduced the side effects associated with cognitive impairment. We evaluated the effects of melatonin on cognition, depressive symptoms and sleep quality, and whether these effects were related to serum levels of Brain Derived Neurotrophic Factor (BDNF) and its receptor, tropomyosin kinase B (TrkB). Thirty-six women were randomly assigned to receive melatonin or placebo for 10 days. To evaluate cognitive performance, we used the Trail-Making-Test Parts A and B (A-B), Rey Auditory-Verbal Learning Test (RAVLT), Controlled Oral Word Association Test (COWAT) and an inhibitory task type Go / No-Go. Our results revealed that melatonin improved executive function on TMT scores, enhanced episodic memory (immediate and delayed) and recognition on RAVLT, and increased verbal fluency in the orthographic COWAT. The TMT-A-B(A-B) were negatively correlated with baseline levels of TrkB and BDNF, respectively. At the end of treatment, changes in TrkB and BDNF were inversely associated with depressive symptoms and sleep quality, but not with the TMT scores. These results suggest a neuroprotective effect of melatonin to counteract the adverse effects of ACBC on cognitive function, sleep quality and depressive symptoms.


Assuntos
Neoplasias da Mama/patologia , Disfunção Cognitiva/prevenção & controle , Depressão/tratamento farmacológico , Melatonina/uso terapêutico , Sono , Adulto , Idoso , Antineoplásicos/uso terapêutico , Biomarcadores/sangue , Fator Neurotrófico Derivado do Encéfalo/sangue , Neoplasias da Mama/complicações , Neoplasias da Mama/tratamento farmacológico , Depressão/etiologia , Método Duplo-Cego , Feminino , Humanos , Melatonina/farmacologia , Glicoproteínas de Membrana/sangue , Pessoa de Meia-Idade , Testes Neuropsicológicos , Efeito Placebo , Receptor trkB/sangue , Sono/efeitos dos fármacos , Resultado do Tratamento
18.
J Med Food ; 23(5): 476-484, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32267780

RESUMO

Post-traumatic stress disorder (PTSD) is a stress-associated mental disorder characterized by an imbalance of neurotransmitters in response to traumatic events or fear. Genistein (GEN), a natural isoflavone, has been shown to exhibit neuroprotective effects. Here, we used the Morris water maze (MWM) and object recognition task (ORT) tests to examine the effects of GEN on cognitive impairment in rats after exposure to single prolonged stress (SPS), and its interaction with the serotonergic system. After exposure to SPS, male rats received GEN (2, 4, and 10 mg/kg, i.p.) for 14 days. Daily GEN administration significantly improved cognitive function in the ORT and MWM tests. GEN treatment also inhibited SPS-induced decreases in serotonin (5-HT) levels in the medial prefrontal cortex and hippocampus. These increased 5-HT concentrations in response to GEN treatment could be partially attributed to the ratio of 5-hydroxyindoleacetic acid/5-HT in the hippocampus. Our findings suggest that GEN significantly attenuates SPS-induced memory deficits in rats and may represent an effective therapeutic option for the treatment of PTSD.


Assuntos
Disfunção Cognitiva/prevenção & controle , Genisteína/uso terapêutico , Transtornos da Memória/prevenção & controle , Serotonina/sangue , Transtornos de Estresse Pós-Traumáticos/tratamento farmacológico , Animais , Cognição/efeitos dos fármacos , Corticosterona/sangue , Modelos Animais de Doenças , Hipocampo/efeitos dos fármacos , Aprendizagem em Labirinto/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Estresse Psicológico
19.
Toxicology ; 436: 152437, 2020 04 30.
Artigo em Inglês | MEDLINE | ID: mdl-32169474

RESUMO

Mild cognitive impairment in Parkinson's disease (PD-MCI) is considered as a nonmotor clinical symptom in Parkinson's disease (PD). Microglia-mediated inflammation contributes to cognitive function impairment. Poloxamer 188 (P188) is an amphipathic polymer which has cytoprotective effect in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced dopaminergic (DA) neurons degeneration in PD. But whether P188 could ameliorate cognitive impairment in PD is still illusive. In the present study, we showed in a mouse model that paraquat (10 mg/kg) and maneb (30 mg/kg) (P + M) treatment intraperitoneally twice a week for 6 consecutive weeks resulted in cognitive deficits and synapse loss in hippocampus, together with DA neuron damage in the substantia nigra pars compacta (SNpc). P188 (0.8 g/kg) injection via tail vein 30 min after P + M administration significantly restored DA neuron numbers in SNpc and synapse density in hippocampus, and alleviated P + M-mediated cognitive function impairment in novel object recognition task and morris water maze task (MWM). Pathological synapse loss might be attributed to increased microglial phagocytic activity and cell density, and P188 prevented P + M-induced phagocytic state changes of microglia, such as increase in cell body size and decrease in process length, and upregulated microglia abundance in hippocampus. Consistently, P188 attenuated P + M-mediated increased mRNA levels of microglia proliferation related CSF1r and CSF2ra, microglial engulfment associated CD68, ICAM1, and ICAM2, and pro-inflammatory IL-6, IL-1ß, CD11b, and TNF-α in hippocampus. Together, these findings suggest that the biocompatible polymer P188 blunts microglia activation which may promote synaptic loss and exacerbate cognitive function in a mouse model of PD-MCI.


Assuntos
Anti-Inflamatórios/farmacologia , Comportamento Animal/efeitos dos fármacos , Cognição/efeitos dos fármacos , Disfunção Cognitiva/prevenção & controle , Hipocampo/efeitos dos fármacos , Mediadores da Inflamação/metabolismo , Transtornos Parkinsonianos/tratamento farmacológico , Parte Compacta da Substância Negra/efeitos dos fármacos , Poloxâmero/farmacologia , Animais , Proliferação de Células/efeitos dos fármacos , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/metabolismo , Disfunção Cognitiva/psicologia , Modelos Animais de Doenças , Neurônios Dopaminérgicos/efeitos dos fármacos , Neurônios Dopaminérgicos/metabolismo , Neurônios Dopaminérgicos/patologia , Hipocampo/metabolismo , Hipocampo/patologia , Masculino , Maneb , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos Endogâmicos C57BL , Microglia/efeitos dos fármacos , Microglia/metabolismo , Microglia/patologia , Degeneração Neural , Paraquat , Transtornos Parkinsonianos/induzido quimicamente , Transtornos Parkinsonianos/metabolismo , Transtornos Parkinsonianos/psicologia , Parte Compacta da Substância Negra/metabolismo , Parte Compacta da Substância Negra/patologia , Fagocitose/efeitos dos fármacos , Poloxâmero/farmacocinética , Reconhecimento Psicológico/efeitos dos fármacos , Sinapses/efeitos dos fármacos , Sinapses/metabolismo , Sinapses/patologia
20.
Clin Sci (Lond) ; 134(7): 765-776, 2020 04 17.
Artigo em Inglês | MEDLINE | ID: mdl-32219335

RESUMO

BACKGROUND: In order to modulate microglial phenotypes in vivo, M1 microglia were depleted by administration of gadolinium chloride and the expression of M2 microglia was induced by IL-4 administration in an animal model of sepsis to better characterize the role of microglial phenotypes in sepsis-induced brain dysfunction. METHODS: Wistar rats were submitted to sham or cecal ligation and perforation (CLP) and treated with IL-4 or GdCl3. Animals were submitted to behavioral tests 10 days after surgery. In a separated cohort of animals at 24 h, 3 and 10 days after surgery, hippocampus was removed and cytokine levels, M1/M2 markers and CKIP-1 levels were determined. RESULTS: Modulation of microglia by IL-4 and GdCl3 was associated with an improvement in long-term cognitive impairment. When treated with IL-4 and GdCl3, the reduction of pro-inflammatory cytokines was apparent in almost all analyzed time points. Additionally, CD11b and iNOS were increased after CLP at all time points, and both IL-4 and GdCl3 treatments were able to reverse this. There was a significant decrease in CD11b gene expression in the CLP+GdCl3 group. IL-4 treatment was able to decrease iNOS expression after sepsis. Furthermore, there was an increase of CKIP-1 in the hippocampus of GdCl3 and IL-4 treated animals 10 days after CLP induction. CONCLUSIONS: GdCl3 and IL-4 are able to manipulate microglial phenotype in an animal models of sepsis, by increasing the polarization toward an M2 phenotype IL-4 and GdCl3 treatment was associated with decreased brain inflammation and functional recovery.


Assuntos
Anti-Inflamatórios/farmacologia , Comportamento Animal/efeitos dos fármacos , Cognição/efeitos dos fármacos , Disfunção Cognitiva/prevenção & controle , Encefalite/prevenção & controle , Gadolínio/farmacologia , Hipocampo/efeitos dos fármacos , Interleucina-4/farmacologia , Microglia/efeitos dos fármacos , Sepse/tratamento farmacológico , Animais , Antígeno CD11b/metabolismo , Proteínas de Transporte/metabolismo , Disfunção Cognitiva/metabolismo , Disfunção Cognitiva/patologia , Disfunção Cognitiva/psicologia , Citocinas/metabolismo , Modelos Animais de Doenças , Encefalite/metabolismo , Encefalite/patologia , Encefalite/fisiopatologia , Hipocampo/metabolismo , Hipocampo/patologia , Hipocampo/fisiopatologia , Mediadores da Inflamação/metabolismo , Microglia/metabolismo , Microglia/patologia , Óxido Nítrico Sintase Tipo II/metabolismo , Fenótipo , Ratos Wistar , Sepse/metabolismo , Sepse/patologia , Sepse/fisiopatologia , Fatores de Tempo
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