Spatial memory impairment without apoptosis induced by the combination of beta-amyloid oligomers and cerebral ischemia is related to decreased acetylcholine release in rats.
Spatial memory impairment without apoptosis induced by the combination of beta-amyloid oligomers and cerebral ischemia is related to decreased acetylcholine release in rats.
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β-淀粉样蛋白寡聚体和脑缺血联合诱导的空间记忆损伤（不伴有细胞凋亡）与大鼠乙酰胆碱释放减少有关。
DOI：
10.1254/jphs.fp0071648
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发表时间：
2008
影响因子：
3.5
通讯作者：
M. Fujiwara
中科院分区：
文献类型：
--
作者：
Takuya Watanabe;K. Iwasaki;Shin Ishikane;Tetsuya Naitou;Y. Yoshimitsu;N. Yamagata;M. B. Ozdemir;Kotaro Takasaki;N. Egashira;K. Mishima;M. Fujiwara
本研究的目的是检查β-淀粉样蛋白（Abeta）寡聚体，而不是纤维，使Abeta斑块，对大鼠的空间记忆和胆碱能系统的影响。最近，一些研究人员提出，Abeta的小组件，Abeta寡聚体，在阿尔茨海默病的早期阶段导致记忆丧失，而没有显示细胞死亡。在本研究中，Abeta寡聚体和脑缺血的组合，而不是单独的脑缺血，显著损害了海马CA 1区的空间记忆，而没有凋亡。乙酰胆碱酯酶抑制剂多奈哌齐可改善这种记忆障碍。因此，我们研究了乙酰胆碱（ACh）释放背海马。微透析研究表明，A β寡聚体和脑缺血的组合并没有显着降低ACh的自发释放;然而，高K（+）诱发的ACh释放减少。这些结果表明，Abeta寡聚体和脑缺血的组合通过胆碱能突触功能障碍诱导记忆障碍，而没有细胞凋亡。该模型可能有助于开发治疗早期阿尔茨海默病的新药。
The purpose of the present study was to examine the effect of beta-amyloid (Abeta) oligomers, not the fibrils that make up Abeta plaques, on spatial memory and the cholinergic system in rats. Recently, several researchers have suggested that small assemblies of Abeta, Abeta oligomers, caused memory loss during the early stages of Alzheimer's disease without showing cell death. In the present study, the combination of Abeta oligomers and cerebral ischemia, but not cerebral ischemia alone, significantly impaired spatial memory without apoptosis in the CA1 region of the hippocampus. Donepezil, an acetylcholinesterase inhibitor, ameliorated this memory impairment. Therefore we examined acetylcholine (ACh) release from the dorsal hippocampus. A microdialysis study showed that spontaneous release of ACh was not significantly decreased by the combination of Abeta oligomers and cerebral ischemia; however, high K(+)-evoked ACh release was decreased. These results suggest that a combination of Abeta oligomers and cerebral ischemia induces memory impairment by cholinergic synapse dysfunction without apoptosis. This model may be useful for developing new drugs for the treatment of early-phase Alzheimer's disease.
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DOI：
10.1001/jama.1997.03540340047031
发表时间：
1997-03-12
影响因子：
120.7
作者：
Snowdon, DA;Greiner, LH;Markesbery, WR
通讯作者：
Markesbery, WR
DOI：
10.1073/pnas.91.8.3270
发表时间：
1994-04-12
影响因子：
11.1
作者：
HENSLEY, K;CARNEY, JM;BUTTERFIELD, DA
通讯作者：
BUTTERFIELD, DA
影响因子：
82.9
作者：
I. Klyubin;D. Walsh;C. Lemere;W. K. Cullen;G. Shankar;V. Betts;E. Spooner;Liying Jiang;R. Anwyl;D. Selkoe;M. Rowan
通讯作者：
I. Klyubin;D. Walsh;C. Lemere;W. K. Cullen;G. Shankar;V. Betts;E. Spooner;Liying Jiang;R. Anwyl;D. Selkoe;M. Rowan
DOI：
--
发表时间：
2001
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
T. Kawarabayashi;L. Younkin;T. Saido;M. Shoji;K. Ashe;S. Younkin
通讯作者：
T. Kawarabayashi;L. Younkin;T. Saido;M. Shoji;K. Ashe;S. Younkin
DOI：
10.1073/pnas.91.25.12243
发表时间：
1994-12-06
影响因子：
11.1
作者：
LORENZO, A;YANKNER, BA
通讯作者：
YANKNER, BA