During his PhD research, Dr. Alexander Jais identified the enzyme heme oxygenase-1 (HO-1) as a strong positive predictor of metabolic disease by intersecting patient data with genetic evidence from five tissue-specific HO-1 deletion mouse models (Jais et al., Cell 2014). His research identified a novel pathomechanism in obesity-induced inflammation, and these results have substantial implications for the stratification of healthy and unhealthy obesity, highlighting the prognostic value of HO-1 for detecting early disease onset. During his postdoctoral research, he revealed that HFD feeding suppresses glucose transporter (GLUT)-1 expression in vascular endothelial cells of the blood-brain barrier, evoking a compensatory recruitment of endothelial-associated macrophages to release VEGF to counteract downregulated GLUT-1 expression (Jais et al., Cell 2016). These findings suggest that metabolic inflammation may develop as a compensatory mechanism to restore transiently reduced brain glucose availability upon consumption of a hypercaloric palatable HFD. Furthermore, he demonstrated that prepronociceptin (PNOC)-expressing neurons in the ARC are activated upon HFD consumption to promote hyperphagia, making them an attractive target for the treatment of obesity and associated metabolic diseases (Jais et al., Neuron 2020).

During his PhD and postdoctoral research, Dr. Jais also participated in highly collaborative projects that led to groundbreaking discoveries, such as the identification of the anaplastic lymphoma kinase (ALK) as a thinness gene and the characterization of a critical role for the enzyme cofactor tetrahydrobiopterin (BH4) in T cell biology (Orthofer et al., Cell 2020; Cronin et al., Nature 2018).

Dr. Alexander Jais expertise lies at the intersection of neurobiology, metabolism and immunometabolism. His work focuses on uncovering the mechanisms by which the central nervous system (CNS) regulates energy balance, glucose homeostasis and metabolic health.