Role of nitric oxide in the aβ25-35 toxicity in vivo

被引：0

作者：

Limon, I. D. ^{[1
]}

Diaz, A. ^{[1
,2
]}

Mendieta, L. ^{[1
]}

Guzman, A. ^{[2
]}

Martinez, I ^{[1
]}

Espinosa, B. ^{[4
]}

Zenteno, E. ^{[3
]}

Guevara, J. ^{[3
]}

机构：

[1] Benemerita Univ Autonoma Puebla, Fac Cs Quim, Lab Neurofarmacol, Puebla, Mexico

[2] INNN MVS, Lab Expt Enfermedades Neurodegenerat, Mexico City, DF, Mexico

[3] Univ Nacl Autonoma Mexico, Fac Med, Dept Bioquim, Mexico City, DF, Mexico

[4] INER, Dept Bioquim, Mexico City, DF, Mexico

来源：

NEW TRENDS IN ALZHEIMER AND PARKINSON RELATED DISORDERS: ADPD 2009 | 2009年

关键词：

OXIDATIVE STRESS; BETA-DEPOSITION; A-BETA; ACTIVATION; AMNESIA; DAMAGE; BRAIN;

D O I：

暂无

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Beta-amyloid plays an important role in the neurodegeneration process of Alzheimer's Disease (AD), but its neurotoxic mechanisms are not clear. It has been associated with the increase of oxidative stress and cognitive impairment because the beta-amyloid peptide 25-35 (A beta((25-35))) has the critical neurotoxic properties of the full-length A beta(1-42). Our present study shows the role of A beta((25-35)), when injected into the hippocampus (Hp) or temporal cortex (TCx), on the nitric oxide (NO) pathways, glial-fibrillary acidic protein (GFAP), 3-nitrotyrosine (3-NT), and the spatial memory of rats one month after the injection. The results showed a significant increase of nitrites in the Hp and TCx of A beta((25-35))-treated rats at the same time that a decrease in the spatial memory and signs of the degeneration process in these areas of the brain occurred. These data suggest that the fraction A beta((25-35)) injected into the Hp or TCx increases NO, which is critical for the neuropathlogical progression and memory impairment in AD.

引用

页码：179 / 185

页数：7

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