LAUSR

Neuronal cell survival, proliferation, and neurogenesis are all dependent on insulin-like growth factor-1/glucagon like peptide-1 (IGF-1/GLP-1) signaling. In the last few decades, the downregulation of IGF-1 and GLP-1 has been linked to problems in the nervous system and these two proteins have become possible therapeutic targets for a number of neurodegenerative and neuropsychiatric disorders. Consequentially, activation of the IGF-1/GLP-1 receptor may play a vital role in neuronal protection. In their review, Bhalla et al . [1] put toge-ther evidence about how IGF-1 and GLP-1 signaling target activators could be used to treat neurological disorders. The analogy of IGF-1 and GLP-1 cross the blood – brain barrier and perform neuroprotective functions such as synaptic formation, neuronal plasticity, protein synthesis, and autophagy. A growing body of literature suggests that disturbance of these pathways contributes to the progressive loss of neurons in the two most common neurodegenerative disorders, Alzheimer ’ s disease (AD) and Parkinson ’ s disease (PD). These fi ndings have prompted numerous studies in preclinical models of neurodegenerative disorders using currently available antidiabetics to target insulin, IGF-1, and GLP-1 signaling. These studies indicate that insulin, IGF-1, and GLP-1 agonists fi x signaling problems and improve surrogate markers of neurodegeneration as well as behavioral outcomes. Several proof-of-concept studies are currently underway to try to apply promising preclinical