Study indicates that the hippocampus mediates cognitive decline in Huntington's disease
Huntington's disease is a neurodegenerative disorder that results in involuntary spastic movement and loss control of voluntary motor function. Patients also exhibit a decline in cognitive ability. The defects in learning and memory associated with Huntington's disease have been ascribed to pathology in the frontal lobe of the brain.
A new study in the Journal of Clinical Investigation suggests that alterations in the hippocampus contribute to memory dysfunction in Huntington's disease.
Silvia Gines and colleagues at the University of Barcelona found increased expression of a protein, p75NTR, in the hippocampus of Huntington's disease patients and mouse models of this disorder. p75NTR is known to reduce dendritic spine density, which is associated with memory and learning defects. Reduction of p75NTR in mouse models of Huntington's disease prevented the cognitive decline and maintained spine density.
Moreover, over expression of p75NTR in the hippocampus of wild type mice recapitulated memory and learning defects associated with Huntington's disease.
The results of this study recognize a potential role of the hippocampus in the development of Huntington's disease.