Amelioration by nitric oxide (NO) mimetics on neurobehavioral and biochemical changes in experimental model of Alzheimer’s disease in rats

A Comparative Study of the Impact of NO-Related Agents on MK-801- or Scopolamine-Induced Cognitive Impairments in the Morris Water Maze

“…A few papers indicated that L-NAME, an NOS inhibitor, disrupted radial water maze learning when given alone or reversed ketamine-induced deficits, depending on the dose [ 28 , 33 ], indicating that NO activation might be essential for water maze learning. Other researchers showed that s-nitrosoglutathione (GSNO), a nitrosothiol, and a sustained NO releaser ameliorated behavioural and neurochemical changes in an experimental model of sporadic Alzheimer‘s disease (sAD) in rats [ 34 , 35 ]. The studies of Wass et al indicated that the administration of a non-selective inhibitor of nitric oxide synthases, l-NAME, alleviated PCP-induced changes in the MWM [ 36 , 37 , 38 ].…”

Blood–Brain Barrier Permeable and NO-Releasing Multifunctional Nanoparticles for Alzheimer’s Disease Treatment: Targeting NO/cGMP/CREB Signaling Pathways

“…Yield 35%. 1 (19). To a solution of compound 18 (1.0 g, 0.35 mmol) and compound 13 (144.9 mg, 0.35 mmol) in MeOH (10 mL) were subsequently added cupric acetate (0.1 equiv) and Vitamin C (0.2 equiv) at room temperature.…”

“…The nitric oxide (NO)/cyclic guanosine monophosphate (cGMP)/cAMP-responsive element-binding protein (CREB) signaling pathway plays important roles in learning and memory formation. − Intrinsic relationships among NO, cGMP, and CREB phosphorylation (p-CREB) were found in synaptic plasticity and memory formation. , Soluble guanylyl cyclase (sGC) stimulators (e.g., NO donor), cGMP-analogues (e.g., 8-bromo-cGMP), or phosphodiesterase 5 (PDE 5) inhibitors can reverse the Aβ-induced impairment of CA1 long-term potentiation (LTP) and improve synaptic function and memory. ,, These findings showed that the upregulation of the NO cascade has favorable results in terms of alleviating synaptic plasticity and memory impairments induced by neurotoxins, such as Aβ oligomers. Indeed, at low levels, NO can react with metals, lipid radicals, and DNA radicals.…”

Citrulline supplementation improves spatial memory in a murine model for Alzheimer's disease

“…NO has been shown to be biologically active in the central nervous system and is involved in learning processes and cognitive function (Hawkins, 1996) as it helps to regulate synaptic plasticity (Dubey et al, 2018) and contributes to long-term potentiation and long-term depression (C. Liu et al, 2019). Deficiency of NO has been implicated in neurodegeneration by promoting endothelial dysfunction, accelerating formation and accumulation of amyloid peptides, reducing synaptic plasticity, activating microglia, and evoking neuroinflammation (Dubey et al, 2018;Katusic & Austin, 2014).…”