Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-β Deposition and Acute Cognitive Deficits in Mice
Traumatic Brain Injury by Weight-Drop Method Causes Transient Amyloid-β Deposition and Acute Cognitive Deficits in Mice
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失重法造成的创伤性脑损伤导致小鼠短暂淀粉样蛋白沉积和急性认知缺陷
作者：
Hajime Shishido;M. Ueno;Kana Sato;Masahisa Matsumura;Yasunori Toyota;Y. Kirino;T. Tamiya;N. Kawai;Y. Kishimoto
越来越多的人意识到创伤性脑损伤（TBI）与老年痴呆症（AD）的发展之间的相关性。已有研究表明，TBI可加速AD模型小鼠的β淀粉样蛋白（Aβ）病理改变和认知功能下降。然而，在野生型（WT）小鼠中，通过重量下降法的TBI对淀粉样蛋白-β病理学和认知表现的短期和长期影响尚不清楚。因此，我们研究了野生型C57 BL 6 J小鼠TBI后AD相关的组织病理学变化和认知障碍。5至7个月大的WT小鼠通过重量下降法或假治疗进行TBI。TBI后7天，WT小鼠的空间学习能力显著低于假手术治疗的WT小鼠。然而，TBI后28天，TBI治疗的WT小鼠的认知障碍恢复。相应地，虽然在TBI后7天在TBI处理的小鼠海马中观察到显著的淀粉样蛋白-β（Aβ）斑块和淀粉样蛋白前体蛋白（APP）积累，但在TBI后28天Aβ沉积不再明显。因此，TBI在WT小鼠中诱导瞬时淀粉样蛋白-β沉积和急性认知障碍。目前的研究表明，TBI可能是急性认知障碍的危险因素，即使不涉及遗传和遗传倾向。该系统可能是有用的评估和开发急性认知功能障碍的药物治疗。
There has been growing awareness of the correlation between an episode of traumatic brain injury (TBI) and the development of Alzheimer's disease (AD) later in life. It has been reported that TBI accelerated amyloid-β (Aβ) pathology and cognitive decline in the several lines of AD model mice. However, the short-term and long-term effects of TBI by the weight-drop method on amyloid-β pathology and cognitive performance are unclear in wild-type (WT) mice. Hence, we examined AD-related histopathological changes and cognitive impairment after TBI in wild-type C57BL6J mice. Five- to seven-month-old WT mice were subjected to either TBI by the weight-drop method or a sham treatment. Seven days after TBI, the WT mice exhibited significantly lower spatial learning than the sham-treated WT mice. However, 28 days after TBI, the cognitive impairment in the TBI-treated WT mice recovered. Correspondingly, while significant amyloid-β (Aβ) plaques and amyloid precursor protein (APP) accumulation were observed in the TBI-treated mouse hippocampus 7 days after TBI, the Aβ deposition was no longer apparent 28 days after TBI. Thus, TBI induced transient amyloid-β deposition and acute cognitive impairments in the WT mice. The present study suggests that the TBI could be a risk factor for acute cognitive impairment even when genetic and hereditary predispositions are not involved. The system might be useful for evaluating and developing a pharmacological treatment for the acute cognitive deficits.
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影响因子：
4.2
作者：
Patricia M. Washington;Nicholas Morffy;Maia Parsadanian;David N Zapple;Mark P. Burns
通讯作者：
Patricia M. Washington;Nicholas Morffy;Maia Parsadanian;David N Zapple;Mark P. Burns
影响因子：
4.1
作者：
MARMAROU, A;FODA, MAA;DEMETRIADOU, K
通讯作者：
DEMETRIADOU, K
影响因子：
4.2
作者：
Carbonell, WS;Maris, DO;Grady, MS
通讯作者：
Grady, MS
DOI：
10.1016/j.jalz.2017.11.007
发表时间：
2018-04
期刊：
Alzheimer's & dementia : the journal of the Alzheimer's Association
影响因子：
--
作者：
Becker RE;Kapogiannis D;Greig NH
通讯作者：
Greig NH