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.
Deciphering the pathogenesis and therapeutic vulnerabilities of pediatric high-grade glioma
Defining mechanisms of skeletal muscle aging, protein homeostasis, and myokines
Examining the coordination of proliferation and differentiation during development and disease
Investigating the molecular mechanisms of cancer metastasis and how they are impacted by host-tumor cell interactions.
Interrogating the biology of pediatric brain tumors and developing preclinical models for therapeutic development
Deciphering control of neuronal death and differentiation
Leveraging multi-omic bulk and single-cell approaches to decipher molecular landscapes and developmental origins of medulloblastoma
Using mass spectrometry-based proteomics, metabolomics and systems biology to understand human disease
Studying high risk pediatric solid tumors
Investigating the neural circuits, synaptic function, and molecular mechanisms controlling learning and memory and their dysfunction in neuropsychiatric disease
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.