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1.
Front Aging Neurosci ; 14: 833365, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-35401157

RESUMEN

Objectives: We evaluated the effects of long-term/recurrent use of antibiotics in childhood on developing cognitive impairment in middle and old age from UK Biobank Database. Methods: UK Biobank recruited participants aged 37-73 years. Cognitive impairment was ascertained by fluid intelligence questionnaire. Primary outcome was the occurrence of cognitive impairment in middle and old age. Multivariate logistic regression models were used to explore the relationship between long-term/recurrent use of antibiotics and cognitive impairment. Results: Over 3.8-10.8 years' follow-up, 4,781 of the 35,921 participants developed cognitive impairment. The odds of cognitive impairment in middle and old age among long-term/recurrent use of antibiotics in childhood were increased by 18% compared with their counterparts (adjusted odd ratio 1.18, 95% confidence interval 1.08-1.29, p < 0.01). The effect of long-term/recurrent use of antibiotics in childhood on cognitive impairment was homogeneous across different categories of various subgroup variables such as sex, age, APOE4, ethnic groups, income before tax, smoking status, alcohol status, BMI, hypertension and diabetes but the effect of long-term/recurrent use of antibiotics in childhood was modified by the educational qualification (p-value for interaction <0.05). Conclusion: Long-term/recurrent use of antibiotics in childhood may increase the risk of cognitive impairment in middle and old age.

2.
Neural Regen Res ; 17(3): 643-648, 2022 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-34380905

RESUMEN

It remains unclear whether limitations in activities of daily living (ADL) increase the risk of stroke in older Chinese adults. This longitudinal study used data from the Chinese Longitudinal Healthy Longevity Survey to investigate the effects of limitations in ADL on the incidence of stroke in older adults. Between 2002 and 2011, 46,728 participants from 22 provinces in China were included in this study. Of participants, 11,241 developed limitations in ADL at baseline. A 3-year follow-up was performed to determine the incidence of stroke. During the 3-year follow-up, 929 participants (8.26%) and 2434 participants (6.86%) experienced stroke in the ADL limitations group and non-ADL limitations group, respectively. Logistic regression was used to analyze the effect of ADL limitations on the risk of stroke. The results showed that after adjusting for the confounding factors gender, age, weight, hypertension, diabetes, heart disease, natural teeth, hearing impairment, visual impairment, smoking, alcohol abuse, exercise, ethnicity, literacy, residential area, and poverty, the ADL limitations group had a 77% higher risk of developing stroke than the non-ADL limitations group. After propensity score matching, the ADL limitations group still had a 33% higher risk of developing stroke than the non-ADL limitations group (OR = 1.326, 95% CI: 1.174-1.497). These findings suggest that limitations in ADL are a stroke risk factor.

3.
J Cell Physiol ; 235(5): 4843-4855, 2020 05.
Artículo en Inglés | MEDLINE | ID: mdl-31663118

RESUMEN

Outer membrane vesicles (OMVs) are nanosized vesicles produced by the gut microbiota (GM). The GM is well-known to be involved in the pathological process of Alzheimer's disease (AD). However, the mechanism of OMVs is not clear. In the present study, we demonstrated the involvement of OMVs in the development of cognitive (learning and memory) dysfunction induced by blood-brain barrier (BBB) disruption. More important, further study showed that OMVs induced tau phosphorylation by activating glycogen synthase kinase 3ß (GSK-3ß) in the hippocampus. OMVs activated astrocytes and microglia, increased secretion of inflammatory cytokines (nuclear factor κB, interleukin-1ß, and tumour necrosis factor-α) in the hippocampus. Therefore, OMVs increase the permeability of the BBB and promote the activation of astrocytes and microglia, inducing an inflammatory response and tau hyperphosphorylation by activating the GSK-3ß pathway and finally leading to cognitive impairment.


Asunto(s)
Membrana Externa Bacteriana/trasplante , Conducta Animal , Encéfalo/metabolismo , Cognición , Disfunción Cognitiva/metabolismo , Vesículas Extracelulares/trasplante , Proteínas tau/metabolismo , Anciano , Animales , Membrana Externa Bacteriana/metabolismo , Encéfalo/patología , Estudios de Casos y Controles , Disfunción Cognitiva/microbiología , Disfunción Cognitiva/patología , Disfunción Cognitiva/psicología , Citocinas/metabolismo , Modelos Animales de Enfermedad , Vesículas Extracelulares/metabolismo , Heces/microbiología , Femenino , Microbioma Gastrointestinal , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Humanos , Masculino , Memoria , Ratones Endogámicos C57BL , Persona de Mediana Edad , Prueba del Laberinto Acuático de Morris , Fosforilación
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