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1.
Artigo em Inglês | MEDLINE | ID: mdl-32741311

RESUMO

With ageing mental health issues, as age-related cognitive decline, increase. This study aims to evaluate the prevalence of cognitive impairment among older European adults and to evaluate its association with clinical and sociodemographic variables, using SHARE. Numeracy, temporal orientation, verbal fluency, and memory were the measures used to evaluate cognitive performance. From 44 963 individuals included, mean age was 70.0±9.0 years old and 56.3% were female. Overall prevalence of impairment was of 13.0% (temporal orientation), 24.8% (numeracy), 27.6% (verbal fluency) and 50.5% (memory). Men showed higher impairment prevalence in temporal orientation and memory and lower in numeracy and verbal fluency. Age, fewer years of education, difficulties performing iADLs, physical inactivity, and poor self-perceived health were independently associated with impairment in all cognitive abilities. These results showed the burden of cognitive impairment across Europe. Factors identified as associated should be taken in consideration to develop effective interventions to prevent cognitive decline.


Assuntos
Envelhecimento , Disfunção Cognitiva/epidemiologia , Idoso , Idoso de 80 Anos ou mais , Bases de Dados Factuais , Europa (Continente)/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prevalência
2.
Cell ; 182(2): 388-403.e15, 2020 07 23.
Artigo em Inglês | MEDLINE | ID: mdl-32615087

RESUMO

Synapse remodeling is essential to encode experiences into neuronal circuits. Here, we define a molecular interaction between neurons and microglia that drives experience-dependent synapse remodeling in the hippocampus. We find that the cytokine interleukin-33 (IL-33) is expressed by adult hippocampal neurons in an experience-dependent manner and defines a neuronal subset primed for synaptic plasticity. Loss of neuronal IL-33 or the microglial IL-33 receptor leads to impaired spine plasticity, reduced newborn neuron integration, and diminished precision of remote fear memories. Memory precision and neuronal IL-33 are decreased in aged mice, and IL-33 gain of function mitigates age-related decreases in spine plasticity. We find that neuronal IL-33 instructs microglial engulfment of the extracellular matrix (ECM) and that its loss leads to impaired ECM engulfment and a concomitant accumulation of ECM proteins in contact with synapses. These data define a cellular mechanism through which microglia regulate experience-dependent synapse remodeling and promote memory consolidation.


Assuntos
Matriz Extracelular/metabolismo , Microglia/fisiologia , Plasticidade Neuronal/fisiologia , Envelhecimento , Animais , Medo , Regulação da Expressão Gênica , Hipocampo/metabolismo , Proteína 1 Semelhante a Receptor de Interleucina-1/genética , Proteína 1 Semelhante a Receptor de Interleucina-1/metabolismo , Interleucina-33/genética , Interleucina-33/metabolismo , Memória , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Neurônios/metabolismo , Transdução de Sinais
3.
Artigo em Coreano | WPRIM (Pacífico Ocidental) | ID: wpr-32196

RESUMO

Arapid increase in the elderly population has raised social awareness for maintaining the health of the elderly and initiated intense research in neurodegenerative diseases. Exercise can improve not only cardiovascular and musculoskeletal fitness, but also suppresses the symptoms of depression and anxiety, suggesting a possible role of exercise in the regulation of brain function. Based on a substantial body of literature, here we introduce the effects of exercise on the structural and functional changes in the aging brain, and also discuss the molecular and cellular effects of exercise and motor learning. Studies show that regular exercise in the elderly promotes neurocognitive function, prevents loss of brain tissue, and reduces the risk for neurodegenerative diseases and brain injury. Although the molecular mechanisms, by which exercise regulates brain function, has not been fully understood, recent cell biological and biochemical studies reveal that exercise increases neurogenesis in the hippocampus, elevates the levels of neurotrophins such as BDNF and IGF-1 to promote the survival of newly generated neurons. Exercise also induces angiogenesis in the motor cortex and cerebellum to enhance delivery of glucose and oxygen to neurons. Furthermore, complex motor skill learning increases the number of synapses to improve cognitive and motor function. Taken together, these findings clearly demonstrate that exercise serves as a behavioral intervention to prevent cognitive decline as well as neurodegenerative diseases. Thus long-term regular exercise in parallel with various learning experiences will be required to prepare successful aging. This study will provide fundamental insights into research in neurodegenerative diseases and a better understanding of the exercise effects in brain function.


Assuntos
Idoso , Humanos , Envelhecimento , Ansiedade , Encéfalo , Lesões Encefálicas , Fator Neurotrófico Derivado do Encéfalo , Cerebelo , Depressão , Glucose , Hipocampo , Fator de Crescimento Insulin-Like I , Aprendizagem , Córtex Motor , Destreza Motora , Fatores de Crescimento Neural , Doenças Neurodegenerativas , Neurogênese , Neurônios , Oxigênio , Sinapses
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