Abnormal brain metabolism as a biomarker for evaluating therapeutic approaches in Huntington’s disease

Author:

Parievsky Anna1,Cepeda Carlos1,Levine Michael S2

Affiliation:

1. IDDRC Room 58-258, Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine, 760 Westwood Plaza, Los Angeles, CA 90095, USA

2. IDDRC Room 58-258, Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine, 760 Westwood Plaza, Los Angeles, CA 90095, USA.

Abstract

Evaluation of: Cepeda-Prado E, Popp S, Khan U, Stefanov D et al. R6/2 Huntington’s disease mice develop early and progressive abnormal brain metabolism and seizures. J. Neurosci. 32, 6456–6467 (2012). In a recent article, Cepeda-Prado et al. use novel and groundbreaking functional MRI methods to elucidate functional, structural and metabolic alterations in the R6/2 mouse model of Huntington’s disease. Based on changes in relative cerebral blood volume, neuronal activity, oxygen and glucose utilization, the authors suggest that R6/2 mice have impaired neurometabolic coupling. They propose the use of relative cerebral blood volume as a biomarker of Huntington’s disease progression, providing a basis for future research examining functional alterations in animal models.

Publisher

Future Medicine Ltd

Subject

Clinical Neurology,Neurology

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