この研究は、高周波電磁界と超音波の共照射(UAHFEMF)がラットおよびマウスの脳に与える変化を観察した。その結果、最大2454時間の照射を受けたラットおよびマウスに、神経突起プラーク、ベータアミロイド、TAUのプラークと細胞内沈着、神経原線維変化(神経細胞内に対のらせん状神経フィラメント(PHF)が凝縮した構造物)などを含む、アルツハイマー病(AD)の特徴的変性が観察された;6匹のマウスで実施した受動的回避テストでは、全てのマウスが、視覚および聴覚失認および脅迫条件認知の喪失の兆候を示した;その後に実施したアミロイド検出用蛍光色素チオフラビンSを用いた顕微鏡法により、脳室拡大およびCa3と歯状回におけるで高密度アミロイド沈着が観察された;UAHFEMF処置を受けたラットの脳に誘導されたヒトT細胞活性化のRhoGTPase活性化タンパク質(TAGAP)のアイソフォームb同族体が、液体クロマトグラフィ・タンデム質量分析法により同定された、などの知見を報告している。
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This study was performed to determine whether the exposure to ultrasound associated with high frequency electromagnetic field (UAHFEMF) can influence the murine behavior and cause histopathological changes characteristic for Alzheimer's disease.
Eight male rats (average weight: 200-250 grams) and 80 male mice (average weight: 30 grams) were used.
The mice underwent the so called passive avoidance test to examine their behavioral changes. They were placed in the light chamber and then let the mice enter in the dark chamber to get an electric shock. Naturally mice flee into the dark chamber because of their inborn light phobic habit. 24 hours later this test was repeated by measuring the time between the been placed in the light chamber and entry the dark chamber. In this way a statement can be made about the avoidance of mice to re-enter the dark chamber und their loss of fear in the light chamber.
ばく露 | パラメータ |
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ばく露1:
27.12 MHz
ばく露時間:
intermittent, max 30 min on/5 min off, less than 12 h/day, total exposure duration up to 2454 h (928 h, 1000 h, 1644 h or 2148 h)
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周波数 | 27.12 MHz |
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タイプ |
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ばく露時間 | intermittent, max 30 min on/5 min off, less than 12 h/day, total exposure duration up to 2454 h (928 h, 1000 h, 1644 h or 2148 h) |
ばく露の発生源/構造 |
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チャンバの詳細 | Exposure facility containing five compartments made of insulated plastic material. Each compartment contained 2 animals. The exposure facility was shielded with 1 mm thick grounded copper plate. |
Additional information | Animals exposed to considerably strong EMF that was tested with a 20 cm fluorescent lamp to make alight. |
No parameters are specified for this exposure.
The passive avoidance test was performed on six mice, and all showed signs of visual and auditory agnosia and loss of fear in the light chamber. The post mortal section revelaed dilated ventricles and dense amyloid deposition in hippocampal areas.
Neurodegenerative changes characteristic for Alzheimer's disease could be demonstrated by the histopathological examinations. Further investigations on rat brain proteins identified the RhoGTPase-Activating Protein (TAGAP) which might play an important role in Alzheimer's disease by its function in signal transduction pathway and/or Tau protein formation.
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