2012年12月4日訊 /生物谷BIOON/ --研究人員報(bào)道稱,，一種通常用于治療人類情緒障礙的藥物——鋰（lithium）,，能夠恢復(fù)海馬中的神經(jīng)元再生（neurogenesis）。海馬是與學(xué)習(xí)和記憶密切相關(guān)的一部分大腦,。
唐氏綜合癥（Down syndrome）是一種神經(jīng)退行性疾病,，是遺傳背景明確的智力殘疾的首要原因。在大腦中,，唐氏綜合癥導(dǎo)致神經(jīng)元之間連接的改變及新神經(jīng)元（神經(jīng)元再生）形成的減少,，而神經(jīng)元再生通常發(fā)生于學(xué)習(xí)過程中。
在一項(xiàng)新研究中,，意大利Istituto Italiano di Tecnologia研究所研究員Laura Gasparini領(lǐng)導(dǎo)的團(tuán)隊(duì)報(bào)告稱,，鋰能夠恢復(fù)海馬中的神經(jīng)元再生。鋰也顯著改善了唐氏綜合癥小鼠在情緒學(xué)習(xí),、空間記憶,、事物辨別等測(cè)試任務(wù)中的表現(xiàn)。這些研究結(jié)果表明,，以鋰為基礎(chǔ)的療法,，有望幫助唐氏綜合癥患者的治療。研究結(jié)果已發(fā)表于Journal of Clinical Investigation雜志,。（生物谷bioon.com）
編譯自：Lithium Restores Cognitive Function in Down Syndrome Mice
doi:10.1172/JCI64650
PMC:
PMID:
Lithium rescues synaptic plasticity and memory in Down syndrome mice
Andrea Contestabile, Barbara Greco, Diego Ghezzi, et al
Abstract:Down syndrome (DS) patients exhibit abnormalities of hippocampal-dependent explicit memory, a feature that is replicated in relevant mouse models of the disease. Adult hippocampal neurogenesis, which is impaired in DS and other neuropsychiatric diseases, plays a key role in hippocampal circuit plasticity and has been implicated in learning and memory. However, it remains unknown whether increasing adult neurogenesis improves hippocampal plasticity and behavioral performance in the multifactorial context of DS. We report that, in the Ts65Dn mouse model of DS, chronic administration of lithium, a clinically used mood stabilizer, promoted the proliferation of neuronal precursor cells through the pharmacological activation of the Wnt/β-catenin pathway and restored adult neurogenesis in the hippocampal dentate gyrus (DG) to physiological levels. The restoration of adult neurogenesis completely rescued the synaptic plasticity of newborn neurons in the DG and led to the full recovery of behavioral performance in fear conditioning, object location, and novel object recognition tests. These findings indicate that reestablishing a functional population of hippocampal newborn neurons in adult DS mice rescues hippocampal plasticity and memory and implicate adult neurogenesis as a promising therapeutic target to alleviate cognitive deficits in DS patients.
