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The abnormal accumulation, assembly and deposition of the amyloid β-protein (Aβ) are prominent pathological features of patients with Alzheimer's disease (AD) and related disorders. A number of factors in the brain can influence Aβ accumulation and associated pathologies. The aim of the present study was to determine the consequences of deleting nitric oxide synthase (NOS) 3, the endothelial form of NOS, in Tg-5xFAD mice, a model of parenchymal AD-like amyloid pathology.

Absence of Nitric Oxide Synthase 3 Increases Amyloid &lt;i&gt;β&lt;/i&gt;-Protein Pathology in Tg-5xFAD Mice

Absence of Nitric Oxide Synthase 3 Increases Amyloid <i>β</i>-Protein Pathology in Tg-5xFAD Mice