作者: DC Andrade , C Toledo , HS Díaz , NC Inestrosa , R Del Rio
DOI: 10.1007/S12035-019-01655-0
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摘要: Heart failure (HF) is a major public health issue affecting more than 26 million people worldwide. HF the most common cardiovascular disease in elder population; and it associated with neurocognitive function decline, which represent underlying brain pathology diminishing learning memory faculties. Both impairment are recurrent hospitalization episodes increased mortality rate older people, but particularly when they occur simultaneously. Overall, published studies seem to confirm that patients display functional impairments relating attention, memory, concentration, learning, executive functioning compared age-matched controls. However, little known about molecular mechanisms underpinning decline HF. The present review round step recent evidence related possible mechanism involved establishment of disorders during We will make special focus on cerebral ischemia, neuroinflammation oxidative stress, Wnt signaling, mitochondrial DNA alterations as cognitive Also, we provide an integrative linking pathophysiological hallmarks altered cardiorespiratory control development dysfunction patients. Graphical Abstract Main heart failure. characterized by chronic activation areas responsible for increasing cardiac sympathetic load. In addition, also show impairment, suggesting overall underpin sympathoexcitation may be low output, infarction due mural emboli ischemia or intermittent hypoperfusion has been described CI. while acute norepinephrine (NE) release relevant induce neural plasticity hippocampus, tonic NE exert opposite effects desensitization adrenergic signaling pathway receptor internalization. Enhanced chemoreflex drive source HF, this phenomenon elevates ROS levels induces through breathing instability. Importantly, both stress can vice versa. Then, inflammatory propagate within potentially contribute activation/inhibition key pathways such pathway.