My laboratory is focused on defining the basic molecular events that underlie human neurodegenerative diseases, and using this information to develop new therapeutic strategies. To accomplish these goals, we use a variety of model systems to understand how mutations in specific genes cause diseases such as amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease. As we have begun to decipher the mechanisms of these diseases, we have found common features that implicate common pathways. One of the common features of these disorders is the presence of pathological structures in brain or spinal cord that are composed of misfolded proteins. Recent studies have revealed that the misfolded pathologic proteins in ALS and Alzheimer’s disease can exhibit prion-like properties to mediate the spread of pathology throughout the brain or spinal cord. We are currently focused on understanding the mechanisms by which pathology seems to spread in the nervous system and identify therapies slow this spread.