2001年8月
Oxidative damage is the earliest event in Alzheimer disease
Journal of Neuropathology and Experimental Neurology
- 巻
- 60
- 号
- 8
- 開始ページ
- 759
- 終了ページ
- 767
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- 出版者・発行元
- AMER ASSN NEUROPATHOLOGISTS INC
Recently, we demonstrated a significant increase of an oxidized nucleoside derived from RNA. 8-hydroxyguanosine (8OHG), and an oxidized amino acid. nitrotyrosine in vulnerable neurons of patients with Alzheimer disease (AD). To determine whether oxidative damage is an early- or end-stage event in the process of neurodegeneration in AD, we investigated the relationship between neuronal 80HG and nitrotyrosine and histological and clinical variables. i.e. amyloid-beta (A beta) plaques and neurofibrillary tangles (NFT), as well as duration of dementia and apolipoprotein E (ApoE1) genotype, Our findings show that oxidative damage is quantitatively greatest early in the disease and reduces with disease progression, Surprisingly, we found that increases in AP deposition are associated with decreased oxidative damage. These relationships are more significant in ApoE is an element of4 carriers. Moreover, neurons with NFT show a 40%-56% decrease in relative 80HG levels compared with neurons free of NFT. Our observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation. These findings suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen.
- リンク情報
- ID情報
-
- ISSN : 0022-3069
- Web of Science ID : WOS:000170192200003