RESUMEN
: Our objective was to study the preventive effect of lowering blood pressure (BP) by medication and/or lifestyle changes on incident all-cause dementia, Alzheimer's disease and vascular dementia. In this systematic review, we included randomized controlled trials with a BP-lowering intervention. Of the nine included trials, seven assessed the effect of antihypertensive medication and two of a lifestyle or combined intervention. In the intervention arm, 1041 out of 29â029 (3.6%) participants were diagnosed with dementia compared with 1090 out of 28â653 (3.8%) controls during a median follow-up of 3.9 years [range 2-10], resulting in a pooled risk ratio of 0.93 (95% confidence interval 0.84-1.02; I 16%). Three trials specified dementia subtypes, with no significant effect on Alzheimer's disease or vascular dementia. To conclude, lowering BP by medication and/or lifestyle changes did not lead to a significantly reduced risk of dementia. This appeared independent of dementia subtype.
Asunto(s)
Enfermedad de Alzheimer/prevención & control , Antihipertensivos/uso terapéutico , Demencia Vascular/prevención & control , Antihipertensivos/farmacología , Presión Sanguínea/efectos de los fármacos , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Conducta de Reducción del RiesgoRESUMEN
Cognitive training has been shown to result in improved behavioral performance in normal aging and mild cognitive impairment (MCI), yet little is known about the neural correlates of cognitive plasticity, or about individual differences in responsiveness to cognitive training. In this study, 21 healthy older adults and 14 patients with MCI received five weeks of adaptive computerized working-memory (WM) training. Before and after training, functional Near-Infrared Spectroscopy (fNIRS) was used to assess the hemodynamic response in left and right prefrontal cortex during performance of a verbal n-back task with varying levels of WM load. After training, healthy older adults demonstrated decreased prefrontal activation at high WM load, which may indicate increased processing efficiency. Although MCI patients showed improved behavioral performance at low WM load after training, no evidence was found for training-related changes in prefrontal activation. Whole-group analyses showed that a relatively strong hemodynamic response at low WM load was related to worse behavioral performance, while a relatively strong hemodynamic response at high WM load was related to higher training gain. Therefore, a 'youth-like' prefrontal activation pattern at older age may be associated with better behavioral outcome and cognitive plasticity.
Asunto(s)
Envejecimiento Cognitivo/fisiología , Disfunción Cognitiva/fisiopatología , Disfunción Cognitiva/rehabilitación , Aprendizaje/fisiología , Memoria a Corto Plazo/fisiología , Corteza Prefrontal/fisiopatología , Anciano , Anciano de 80 o más Años , Presión Sanguínea/fisiología , Mapeo Encefálico , Circulación Cerebrovascular/fisiología , Disfunción Cognitiva/psicología , Femenino , Frecuencia Cardíaca/fisiología , Humanos , Masculino , Persona de Mediana Edad , Plasticidad Neuronal/fisiología , Espectroscopía Infrarroja Corta , Resultado del TratamientoRESUMEN
Systemic Lupus Erythematosus is an autoimmune disease characterized by the formation of anti-nuclear autoantibodies, particularly anti-chromatin. Although the aetiology of the disease has not yet been fully elucidated, several mechanisms have been proposed to be involved. Due to an aberrant apoptosis or decreased removal of apoptotic cells, apoptotic blebs containing chromatin are released. During apoptosis, chromatin is modified that increases its immunogenicity. Myeloid dendritic cells (myDC) can take up apoptotic blebs and stimulate autoreactive T helper cells, and subsequently the formation of autoantibodies by autoreactive B cells. Immune complexes formed by anti-chromatin autoantibodies and modified chromatin deposit on basal membranes, and incite a local inflammation, but can also stimulate plasmacytoid dendritic cells to produce IFN-α. In addition to apoptotic blebs, neutrophil extracellular traps released by dying neutrophils, in a process called NETosis, may serve as a source of autoantigens as well. In this review, we describe the role of both apoptosis and NETosis in the pathogenesis of SLE, and show how both processes may interact with each other.