Leptin is a hormone that regulates appetite by acting on receptors in the hypothalamus, where it modifies food intake to maintain equilibrium with the body energy resources. Leptin and its receptors are widely distributed in the central nervous system, suggesting that they may give neuronal survival signals. The potential of leptin to decrease/increase neuronal damage and neuronal plasticity in Parkinson's diseases (PD) is the subject of this review, which outlines our current knowledge of how leptin acts in the brain. Although leptin-mediated neuroprotective signalling results in neuronal death prevention, it can affect neuroinflammatory cascades and also neuronal plasticity which contribute to PD pathology. Other neuroprotective molecules, such as insulin and erythropoietin, share leptin-related signalling cascades, and therefore constitute a component of the neurotrophic effects mediated by endogenous hormones. With the evidence that leptin dysregulation causes increased neuronal vulnerability to damage in PD, using leptin as a target for therapeutic modification is an appealing and realistic option.
Keywords: Parkinson's disease; adipose tissue; inflammation; leptin; neuroprotection.
© 2022 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.