Taken together, the findings suggest that the neurotherapeutic potential of L-NBP as a disease modifier in AD is due to its multiple pharmacological properties. It may be hypothesized from the experimental findings that the specific feature of this compound is the ability to reduce the load of Aβ and to exert anti-oxidant properties by lowering the levels of ROS, maintaining optimum MMP with reduction in inflammatory markers. For the first time Zhang et al. (2016) have demonstrated that this molecule could also repair synaptic damages via modulation of PSD95, synaptophysin (SYN), β-catenin, and GSK-3 β. L-NBP acts through various systems to impede progression of AD. Previous studies with L-NBP in patient with subcortical vascular cognitive impairment without dementia have demonstrated improved cognitive and global functioning and good safety (Jia et al., 2016). Another study by Xiang et al. (2014) also supported the neuroprotective role of L-BNP in an AD model by inhibiting oxidative injury, neuronal apoptosis and glial activation, regulating amyloid-beta protein precursor processing and reducing amyloid-beta formation. These studies substantiate the necessity of further evaluations of L-NBP for its potential beneficial effects in neurological diseases. However, the clinical efficacy of the molecule still requires to be evaluated. Bioavailability is considered as another major issue faced by natural compounds during clinical trials. Until disease-modifying therapies become available, further research is needed to develop new drug delivery strategies to ensure ease of administration and adequate pharmacokinetic properties, since no available treatments stop or reverse the progression of the disease. As of 2016, more than 1000 clinical trials have been or are being conducted to find ways to treat the disease, but it is unknown if any of the tested treatments will work.