Neuron· Julie Ouellette, Sareen Warsi, Phinea Romero, Purva Khare, Shama Naz, Leya Aubert-Tandon, Moises Freitas-Andrade, Chantal Pileggi, Sozerko Yandiev, Joanna Raman-Nair, James Yee, Nicole Blakeley, Balaji Govindaswamy, Cesar Henrique Comin, Mary-Ellen Harper, Devika Soundara Manickam, Fabrice Dabertrand, Armen Saghatelyan, Baptiste Lacoste·· 28 天前AI 评分62
Neuron：16p11.2缺失致脑内皮细胞能量代谢障碍，激活P2Y2受体可改善小鼠行为
Purinergic receptor activation rectifies autism-associated endothelial dysfunction
AI 导读
依据摘要，Ouellette 等报告 16p11.2 缺失会在脑内皮细胞中引发生物能量学障碍，而通过 P2Y2 受体激活嘌呤能信号可恢复内皮功能，并改善携带该缺失的小鼠的行为。研究提示靶向内皮代谢与嘌呤能信号可能成为自闭症的潜在治疗方向。上述结果来自小鼠模型，尚未在人体中验证，不能直接外推为临床疗效。
摘要
Ouellette et al. report that a 16p11.2 deletion induces a bioenergetic failure in brain endothelial cells. Activation of purinergic signaling via P2Y2 receptors restored endothelial function and improved behaviors in mice carrying a 16p11.2 deletion. Targeting endothelial metabolism and purinergic signaling may thus represent a promising therapeutic avenue for autism.
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来源：Neuron · cell.com