It has become amply clear that mitochondrial function defined by quality, 
quantity, dynamics, homeostasis, and regulated by mitophagy and mitochondrial 
biogenesis is a critical metric of human aging and disease. As a consequence, 
therapeutic interventions that can improve mitochondrial function can have a 
profound impact on human health and longevity. Kisspeptins are neuropeptides 
belonging to the family of metastasis suppressors that are known to regulate 
functions like fertility, reproduction, and metabolism. Using SKNSH cell line, 
hippocampus explant cultures and hippocampus of aging Wistar rat models, we show 
that Kisspeptin-10 (Kp) induces autophagy and mitophagy via calcium, 
Ca2+/CaM-dependent protein kinase kinase β (CaMKKβ), AMP-activated protein 
kinase (AMPK), and Unc-51 like autophagy activating kinase (ULK1) signaling 
pathway that is independent of mammalian target of rapamycin (mTOR). 
Intriguingly, Kp administration in vivo also results in the enhancement of 
mitochondrial number, complex I activity, and Adenosine Triphosphate (ATP) 
levels. This study uncovers potential effects of Kp in protecting mitochondrial 
health and as a possible therapeutic intervention to hippocampus associated 
impairments such as memory, cognitive aging, and other diseases linked to 
mitochondrial dysfunction.