With the advent of new diagnostic tools various pathological conditions have been identified at different stages of AD. Accumulation of amyloid beta (Aβ) to form clumps known as neuritic or senile plaques is considered as hallmark of AD. The buildup of these plaques seems to be a crucial as they lead to oxidative stress coupled with mitochondrial dysfunction and barrage of inflammatory cascade causing neuronal cell death. Studies carried by Zhang et al. (2016) on L-3-n-butylphthalide (L-NBP) extracted from seeds of Chinese celery (Apium graveolens Linn) showed some promising results in animal models of AD. Interestingly treatment of L-NBP (15 mg/kg; oral, 3 months) to APP/PS1 mice resulted in amelioration of Aβ induced damage to synapse. Improvement in synaptic plasticity which is considered as an essential factor modulating cognitive functions in AD has also been observed after L-NBP. Pictorial results from electron microscopy revealed the significant increase in number of synapse and spines in hippocampus regions following treatment with L-NBP. It could be reasoned that multiple molecular events have been amended to bring about changes in synaptic strength. These changes might range from removal of synaptic plaques to anti oxidative and anti-inflammatory mechanisms. However, it is very hard to distinguish whether removal of synaptic plaques provides anti oxidative and anti-inflammatory relief or vice versa. In this study Zhang et al. (2016) explored pertinent proteins associated with synaptic plasticity in hippocampus to unveil the mechanism of neuroprotective effects of L-NBP and found upregulation in expression of PSD95, synaptophysin, β-catenin and GSK- 3β on treatment with L-NBP. PDS-95 is an abundant synaptic protein playing an important role in maintaining and regulating excitatory synapses and promoting synaptogenesis. β-catenin is a crucial factor for Wnt signaling pathway necessary for the maintenance of dendritic strength and density. An important issue remaining unanswered in these studies was involvement of adult neurogenesis following exposure to L-NBP. Since it affects multiple pharmacological targets it could be reasoned that L-NBP might alter stem cells in the hippocampal region to bring about changes in synaptic plasticity by involving the Wnt pathway. Whether the potential of L-NBP is limited to the degradation of Aβ or it might regulate proteins associated with adult neurogenesis via activation of stem cell markers in AD still remains elusive (Lei et al., 2014).