Quantitative proteomics of synaptosome S-nitrosylation in Alzheimer's disease.

Increasing evidence suggests that both synaptic loss and neuroinflammation constitute early pathologic hallmarks of Alzheimer's disease. A downstream event during inflammatory activation of microglia and astrocytes is the induction of nitric oxide synthase type 2, resulting in an increased release of nitric oxide and the post-translational S-nitrosylation of protein cysteine residues. Both early events, inflammation and synaptic dysfunction, could be connected if this excess nitrosylation occurs on synaptic proteins.

Proteome profiling of s-nitrosylated synaptosomal proteins by isobaric mass tags.

• Protocol for quantitative proteomics of nitrosylation on synaptosomal proteins. • Identification of endogenous nitrosylation independent of induction by NO donors. • Use of iodoTMT sixplex mass tags for stable labeling, enrichment, identification, and multiplex quantitation.

Water deprivation induces neurovascular and cognitive dysfunction through vasopressin-induced oxidative stress.

Adequate hydration is essential for normal brain function and dehydration induces cognitive deterioration. In addition, dehydration has emerged as a stroke risk factor. However, it is unknown whether alterations in cerebrovascular regulation are responsible for these effects.