Catálogo de publicaciones - revistas

<jats:title>Adult neurogenesis and Alzheimer's disease</jats:title> <jats:p> Alzheimer's disease (AD) pathology destroys neurons and synapses in the brain, leading to dementia. The brain generates new neurons throughout life in the hippocampus, a process called adult hippocampal neurogenesis (AHN). Choi <jats:italic>et al.</jats:italic> found that blocking AHN exacerbated cognitive impairment in an AD mouse model (see the Perspective by Spires-Jones and Ritchie). Inducing neurogenesis alone did not improve cognition in AD mice, whereas inducing neurogenesis while simultaneously ameliorating the neuronal environment via exercise did. The use of genetic or pharmacological treatments that simultaneously induced neurogenesis and increased levels of brain-derived neurotrophic factor (BDNF) mimicked the benefits of exercise on cognition. Thus, inducing both neurogenesis and providing BDNF may be useful as an AD therapeutic. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aan8821">eaan8821</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6406" page="975" related-article-type="in-this-issue" vol="361" xlink:href="10.1126/science.aau8060">975</jats:related-article> </jats:p>

<jats:title>Making sense of transient dynamics</jats:title> <jats:p> Ecological systems can switch between alternative dynamic states. For example, the species composition of the community can change or nutrient dynamics can shift, even if there is little or no change in underlying environmental conditions. Such switches can be abrupt or more gradual, and a growing number of studies examine the transient dynamics between one state and another—particularly in the context of anthropogenic global change. Hastings <jats:italic>et al.</jats:italic> review current knowledge of transient dynamics, showing that hitherto idiosyncratic and individual patterns can be classified into a coherent framework, with important general lessons and directions for future study. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aat6412">eaat6412</jats:related-article> </jats:p>

<jats:title>A complex implicated in kidney health</jats:title> <jats:p> Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disease that can lead to kidney failure. Mutations in the proteins PKD1 and PKD2 are linked to the disease, but the function of these proteins remains unclear, both in physiology and disease. PKD1 has been implicated in the sensing of chemical and mechanical force stimuli, and PKD2 is proposed to be a calcium ion channel. Su <jats:italic>et al.</jats:italic> show that the transmembrane regions form a PKD1-PKD2 complex assembled in a 1:3 ratio. Their high-resolution cryo–electron microscopy structure confirms that the complex adopts transient receptor potential channel architecture, with some distinctive features. Mapping disease-causing mutations onto the structure suggests that pathogenesis may come from incorrect folding or trafficking of the complex rather than from disruption of channel activity. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" related-article-type="in-this-issue" xlink:href="10.1126/science.aat9819">eaat9819</jats:related-article> </jats:p>