Kisspeptin-13 Improves Spatial Memory Consolidation and Retrieval against Amyloid-β Pathology

It has been shown that brain glucose metabolism impairment, obesity, and diabetes couldlead to cognitive decline and Alzheimer’s disease (AD) pathogenesis. Kisspeptin (KP) a G-proteincoupled receptor neuropeptide, has been suggested as a link between energy balance andreproduction. Some studies have shown that the attenuation of KP signaling decreases metabolismand energy expenditure. KP mRNAs and receptors are detected in the hippocampusand cause the promotion of excitatory synaptic responses through modulation of postsynapticsignaling. The purpose of this study was to investigate the effect of KP on spatial learning andmemory and its possible neuroprotective effect on Amyloid-Beta induced cognitive impairmentusing the Morris Water Maze (MWM) task in rats. The reference and reversal spatial learningand memory have been measured in this study. Rats were injected bilaterally by Aβ1-42 (2 μg/μL) or saline as a vehicle into the hippocampal CA1 area. One week later, KP-13 (1.5 or 2 μg/μL) was injected i.c.v before or after each training session for 3 days and memory was tested24 h later. The results showed KP-13 by itself could significantly enhance spatial memoryconsolidation and retrieval, and Aβ induced reversal and reference memory impairment wassignificantly ameliorated by KP-13. In Conclusion, it seems that KP-13 as a neuropeptide hasto enhance spatial memory properties and could be a possible neuroprotective peptide on amyloid-beta induced pathology.