Can we learn about brain function from neurological disease?
We can gain novel insights into nervous system development by studying how it is altered in disease. Most complex neurologic diseases are revealed when an environmental stress intersects with an underlying vulnerability that was otherwise masked. Investigators in DNB are working to understand how chronic and acute stress can impact nervous system function and contribute to neurologic diseases. How does stress affect each cell type and do they signal to each other? Is cellular stress cumulative? How does aging influence these processes? Do different tissues signal to each other during stress? By answering these questions, we will be able to develop new paradigms for initiation and progression of neurologic diseases.
Clinical observations indicate that skeletal muscle influences CNS aging, but the underlying muscle-to-brain signaling remains unexplored. Work from the Demontis lab revealed that moderate perturbation of the proteasome in skeletal muscle induces compensatory preservation of CNS proteostasis during aging through adaptive responses via amylase/maltose.