iNOS gene deficiency modifies beta-amyloid deposition, cognitive performance and hippocampal long term potentiation in APPPS1 tg mice

The inducible form of the nitric oxide synthase (iNOS), is transcriptionally upregulated in response to inflammatory stimuli in Alzheimer's disease, potentially aggravating disease progression. In this study we determined the effect of iNOS deficiency in amyloid precursor protein/presenilin1 (APPPS1) transgenic mice on spatial memory, hippocampal long term potentiation (LTP), amyloid pathology, neuroinflammation and neuronal loss. APPPS1/iNOS (-/-) mice as well as APPPS1 mice treated with the iNOS inhibitor L-NIL, showed a significant reduction of working memory errors in the radial arm maze-test at 3 and 12 mon…