Peggy Nopoulos
Roy J. and Lucille A. Carver College of Medicine
63 Papers
347 Citations
Peggy Nopoulos is an academic researcher from Roy J. and Lucille A. Carver College of Medicine. The author has contributed to research in topics: Medicine & Brain morphometry. The author has an hindex of 27, co-authored 63 publications. Previous affiliations of Peggy Nopoulos include University of Iowa & University of Iowa Hospitals and Clinics.
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Papers
Longitudinal change in regional brain volumes in prodromal Huntington disease
Elizabeth Aylward,Peggy Nopoulos,Christopher A. Ross,Douglas R. Langbehn,Ronald Pierson,James A. Mills,Hans J. Johnson,Vincent A. Magnotta,Andrew R. Juhl,Jane S. Paulsen +9 more
TL;DR: Clinical trials using white matter or striatal volume change as an outcome measure will be most efficient if the sample is restricted to individuals who are within 15 years of estimated onset of diagnosable disease.
263
Gyrification abnormalities in childhood- and adolescent-onset schizophrenia.
Tonya White,Nancy C. Andreasen,Nancy C. Andreasen,Nancy C. Andreasen,Peggy Nopoulos,Vincent A. Magnotta +5 more
TL;DR: Children and adolescents with schizophrenia demonstrated patterns of brain morphology that were distinctly different from healthy controls, and these changes may reflect aberrations in cerebral and subcortical connectivity.
205
Cerebral cortex structure in prodromal Huntington disease.
Peggy Nopoulos,Elizabeth Aylward,Christopher A. Ross,Hans J. Johnson,Vincent A. Magnotta,Andrew R. Juhl,Ronald Pierson,James A. Mills,Douglas R. Langbehn,Jane S. Paulsen +9 more
TL;DR: Cortical volume, thickness, and surface area were not significantly different between the Far from onset group and controls, however, beginning in the Midway to onset group, the cortex showed significant volume decrement, affecting most the posterior and superior cerebral regions.
160
Huntington disease: a single-gene degenerative disorder of the striatum.
TL;DR: As a single-gene disorder, HD has the distinction of having the potential of treatment that is aimed directly at the known pathogenic mechanism by gene silencing, providing hope for neuroprotection and ultimately, prevention.
151
Smaller intracranial volume in prodromal Huntington's disease: evidence for abnormal neurodevelopment
Peggy Nopoulos,Elizabeth Aylward,Christopher A. Ross,James A. Mills,Douglas R. Langbehn,Hans J. Johnson,Vincent A. Magnotta,Ronald Pierson,Leigh J. Beglinger,Martha Nance,Roger A. Barker,Jane S. Paulsen +11 more
TL;DR: The current findings suggest that mutant huntingtin can cause abnormal development, which may contribute to the pathogenesis of Huntington's disease.