Christopher Miller

Chris Miller is in the Department of Basic and Clinical Neuroscience. Work in our research group aims to understand better, the molecular mechanisms that underlie neuronal cell death in neurodegenerative diseases. We are studying Alzheimer’s disease, frontotemporal dementia with related amyotrophic lateral sclerosis (FTD/ALS) and Parkinson’s disease since these neurodegenerative diseases share many pathogenic features and as such there may be common routes for therapy. We are particularly interested in how signaling between the endoplasmic reticulum (ER) and mitochondria might contribute to the neurodegenerative process. This is because ER-mitochondria signaling regulates many of the physiological processes that are damaged in neurodegenerative diseases; these include bioenergetics, mitochondrial function, calcium and lipid homeostasis, ER stress responses, autophagy, axonal transport and inflammation. We have identified mechanisms that mediate ER-mitochondria signaling and have shown that they are damaged in FTD/ALS and Parkinson’s disease. We are currently studying the cell and molecular routes that underlie this damage. These studies involve cell and molecular approaches, transgenic mouse and zebrafish models, and human disease tissues including neurons derived from iPS cells that carry familial pathogenic mutations. Finally, we are seeking pharmacological routes for correcting damaged ER-mitochondria signaling as a novel therapeutic approach for neurodegenerative diseases.

1. Chris Miller is in the Department of Basic and Clinical Neuroscience. Work in our research group aims to understand better, the molecular mechanisms that underlie neuronal cell death in neurodegenerative diseases. We are studying Alzheimer’s disease, frontotemporal dementia with related amyotrophic lateral sclerosis (FTD/ALS) and Parkinson’s disease since these neurodegenerative diseases share many pathogenic features and as such there may be common routes for therapy. We are particularly interested in how signaling between the endoplasmic reticulum (ER) and mitochondria might contribute to the neurodegenerative process. This is because ER-mitochondria signaling regulates many of the physiological processes that are damaged in neurodegenerative diseases; these include bioenergetics, mitochondrial function, calcium and lipid homeostasis, ER stress responses, autophagy, axonal transport and inflammation. We have identified mechanisms that mediate ER-mitochondria signaling and have shown that they are damaged in FTD/ALS and Parkinson’s disease. We are currently studying the cell and molecular routes that underlie this damage. These studies involve cell and molecular approaches, transgenic mouse and zebrafish models, and human disease tissues including neurons derived from iPS cells that carry familial pathogenic mutations. Finally, we are seeking pharmacological routes for correcting damaged ER-mitochondria signaling as a novel therapeutic approach for neurodegenerative diseases.