Dr. DeArmond completed his PhD in 1972 and his MD in 1975 at the Medical College of Pennsylvania. He completed two years of internship and residency training in Anatomic Pathology and three years of Neuropathology fellowship training at Stanford University Medical Center. He is Board certified in both Anatomic Pathology and Neuropathology. Following three years of research of glial fibrillary acidic protein in Lawrence Eng's laboratory at the Palo Alto Veteran's Administration Medical Center and a junior faculty appointment at Stanford, in 1983 he was recruited to the Pathology Department at UCSF to add a research component as well as additional diagnostic support to the Neuropathology Unit.

Although he brought research of astrocytes and glial neoplasms from Stanford, Dr. Stanley Prusiner invited him to add a neuropathology and immunohistochemistry component to his studies of prion diseases, which has led to a close and productive collaboration for over 20 years. The DeArmond Neuropathology Research Laboratory has focused on the cell biological and molecular mechanisms of neurodegeneration in prion diseases. His accomplishments include showing that amyloid plaques in Creutzfeldt-Jakob disease are composed of PrP^Sc and that accumulation of non-amyloid PrP^Sc in the brain is the cause of early synaptic dysfunction and degeneration and the cause of late occurring nerve cell death. Subcellular fractionation studies in his lab have shown that 10 to 50 times more PrP^Sc accumulates in plasma membranes of prion-infected cell lines than the normal cellular isoform, PrP^C. Accumulation of PrP^Sc was found to change the properties of the plasma membrane and alter receptor-mediated transmembrane signaling. More recently, he has been testing whether PrP^Sc accumulation alters expression of genes known to play critical roles in presynaptic and postsynaptic growth and maturation during CNS development. He found a direct correlation between synaptic PrP^Sc accumulation and activation of Notch-1 releasing the Notch-1 intracellular domain (NICD). NICD is a transcription factor that ultimately decreases expression of genes that maintain dendritic and axonal lengths. This finding argues that synapse degeneration in prion diseases is a programmed event (synoptosis) similar to programmed nerve cell death (apoptosis). A clinical implication of this finding is the potential that prevention of Notch-1 activation by pharmaceutical agents might prevent progressive cognitive decline in prion diseases and possibly even in other dementing disorders.

Dr. DeArmond's clinical responsibilities include directing the muscle and nerve diagnostic service, participating in the brain tumor diagnostic service, and covering the autopsy brain cutting service at the UCSF affiliated hospitals. Dr. DeArmond directs several neuropathology cores that are integral components of human and animal prion disease program projects. Most of the cases in these projects undergo a comprehensive quantitative clinical-neurohistological analysis or are part of other funded research questions.