絞り込み

16641

広告

「私たちは変われる」グレタさん COP25で行動を訴える

地球温暖化対策を話し合う国連の会議、「COP25」の会場を訪れているスウェーデンの16歳、グレタ・トゥーンベリさんは、スペインの閣僚らとともに公式イベントに登場...

  1. 読書のために小旅行を: 極東ブログ
  2. COP25で小泉氏「残念ながら」石炭火力...
  3. 小泉環境相、石炭利用「世界的な批判を認識...
  4. 供託金なくしたら「N国」より「過激候補」...

ニュース一覧

S14G-Humanin improves cognitive deficits and reduces amyloid pathology in the middle-aged APPswe/PS1dE9 mice.

著者 Zhang W , Zhang W , Li Z , Hao J , Zhang Z , Liu L , Mao N , Miao J , Zhang L
Pharmacol Biochem Behav.2011 Oct 2 ; ():.
この記事をPubMed上で見るPubMedで表示
この記事をGoogle翻訳上で見る Google翻訳で開く

Department of Neurology, Tangdu Hospital, Fourth Military Medical University, Xi'an City, Shaanxi Province 710038, China.

スターを付ける スターを付ける     (219view , 0users)

Full Text Sources

Medical

Miscellaneous

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by clinical cognitive decline and pathological deposition of amyloid-beta protein (Aβ) in the brain. So far, there has been no causative therapy for this devastating disease. S14G-Humanin (HNG), a synthetic derivative of Humanin (HN), has been shown to have strong neuroprotective ability against AD-related insults in vitro and prevent cognitive impairments in Aβ-infused animal models. In addition, a recent study has reported a beneficial effect of intranasal HNG treatment on memory deficit and Aβ accumulation in triple transgenic (3xTg-AD) mice at the early plaque-bearing stage. However, whether HNG treatment has the disease-modifying efficacy on AD with pre-existing well-established amyloid plaque pathology remains unclear. In this study, we employed 9-month-old APPswe/PS1dE9 mice with pre-existing robust amyloid plaque pathology to investigate the effects of chronic HNG treatment on the progression of cognitive dysfunction and Aβ-associated neuropathology. We found that vehicle-treated APPswe/PS1dE9 mice showed impaired spatial learning and memory compared with vehicle- and HNG-treated wild-type mice, while intraperitoneal HNG treatment for 3months significantly improved spatial learning and memory deficits in APPswe/PS1dE9 mice compared with vehicle control treatment. Coincidental with this, HNG treatment significantly reduced cerebral Aβ plaque deposition, insoluble Aβ levels, and neuroinflammatory responses in APPswe/PS1dE9 mice compared with control treatment. Cumulatively, these findings demonstrate that chronic administration of HNG is able to attenuate cognitive deficits and reduce Aβ loads as well as neuroinflammation in the middle-aged APPswe/PS1dE9 mice even with pre-existing substantial Aβ neuropathology, indicating that HNG has potential as a pharmacotherapeutic intervention in the development of cognitive deficits and neuropathology seen in the cases of established AD.
PMID: 21993310 [PubMed - as supplied by publisher]
印刷用ページを開く Endnote用テキストダウンロード