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Background

Recent research suggests that cerebrovascular endothelial dysfunction during advanced aging, together with other risk factors, may trigger the neurodegenerative processes in Alzheimer's disease (AD). AD brains display dramatically reduced protein expression of endothelial nitric oxide synthase (eNOS) and excessive amounts of ammonia and urea. In eNOS deficient (eNOS−/-) mice, interestingly, there are age-related memory deficits and amyloid accumulation, indicating a potential role of eNOS deficiency in the development of AD. The present study aimed to investigate how ammonia and urea changed in the brain of eNOS deficient mice.

Methods

Using the ammonia and urea kits, we quantified the levels of ammonia and urea in the cortex of male eNOS−/-and wild-type (WT) mice at 4 and 14 months of age.

Results

There was a trend of genotype-related increase in ammonia or urea at younger age …