AI Article Synopsis
- The study aimed to explore how nitric oxide synthase (NOS) and nitric oxide (NO) contribute to neurotoxicity caused by beta-amyloid (Abeta) and the development of Alzheimer's disease (AD).
- Researchers conducted experiments on rats, injecting Abeta(1-40) into their hippocampi and assessing the impacts on learning and memory through behavioral tests, as well as observing changes in brain structure.
- Findings revealed that inhibiting inducible NOS (iNOS) with aminoguanidine (AG) prevented memory impairment and brain damage from Abeta, suggesting that iNOS/NO is crucial in the neurotoxicity linked to Abeta and the progression of AD.
Article Abstract
Aim: To investigate the causative role of nitric oxide synthase (NOS) and nitric oxide (NO) in neurotoxicity of beta-amyloid (Abeta) and the pathogenesis of Alzheimer's disease (AD).
Methods: Using behavioral and neuropathological methods, we observed the effects of Abeta(1-40) injection into hippocampi on rats learning and memory in Y maze and on the neuropathology in hippocampi. The intervention by intraperitoneal administration of aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS (nNOS) inhibitor, in the neurotoxicity of Abeta(1-40) was studied then.
Results: The capability of acquisition and retrieval in Y maze and local neurons in hippocampus of the rats were impaired significantly after Abeta(1-40) injection. Intraperitoneal administration of AG, but not 7-NI, could prevent the damages caused by Abeta(1-40) injection above-mentioned.
Conclusion: iNOS/NO participates in the mechanisms of Abeta-induced neurotoxicity and may play an important role in the pathogenesis of AD.
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