据9月18日的《科学》杂志报道说，对患有Alzheimer氏病的小鼠的脑子进行扫描发现了一类“活动亢进的”神经元，它们与该疾病的症状有关联。这些活动亢进的神经元最密集地集中在病变脑组织中所发现的淀粉样斑块沉积处的附近，而它们的存在可能是癫痫样发作增加的基础。
Marc Aurel Busche及其同僚应用双光子Ca2+ 成像来对受到Alzheimer氏症影响的小鼠脑中正在发生的活动进行检测。他们发现脑组织中有整整一半的神经元的冲动发放速度是在其正常范围之外的——即冲动发放或者太快或者太慢。
研究人员提示，这种亢进是因为突触抑制受到损害引起的，而非因为激发正常神经元冲动发放的Ca2+释放的波动所引起的。他们还说，这种在淀粉样斑块附近的快速发放的活动亢进神经元是以一种互为关联的方式发放冲动的，从而增加了癫痫发生的危险。这种新的Alzheimer病的小鼠模型可以为将来治疗这种疾病提供主意。（生物谷Bioon.com）
生物谷推荐原始出处：
Science 19 September 2008: Vol. 321. no. 5896, pp. 1686 - 1689 DOI: 10.1126/science.1162844
Clusters of Hyperactive Neurons Near Amyloid Plaques in a Mouse Model of Alzheimer's Disease
Marc Aurel Busche,1,4 Gerhard Eichhoff,1,4 Helmuth Adelsberger,1,4 Dorothee Abramowski,2 Karl-Heinz Wiederhold,2 Christian Haass,3,4 Matthias Staufenbiel,2 Arthur Konnerth,1,4* Olga Garaschuk1,4
The neurodegeneration observed in Alzheimer's disease has been associated with synaptic dismantling and progressive decrease in neuronal activity. We tested this hypothesis in vivo by using two-photon Ca2+ imaging in amouse model of Alzheimer's disease. Although a decrease in neuronal activity was seen in 29% of layer 2/3 corticalneurons, 21% of neurons displayed an unexpected increase in the frequency of spontaneous Ca2+ transients. These"hyperactive" neurons were found exclusively near the plaques of amyloid β–depositing mice. The hyperactivityappeared to be due to a relative decrease in synaptic inhibition. Thus, we suggest that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides amechanism for the disturbed cortical function in Alzheimer's disease.
