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BioMed Research International
Volume 2015, Article ID 610605, 13 pages
Research Article

Posterior Cingulate Lactate as a Metabolic Biomarker in Amnestic Mild Cognitive Impairment

1Department of Radiology, University of Washington, P.O. Box 357115, Seattle, WA 98195, USA
2Integrated Brain Imaging Center, University of Washington, Seattle, WA 98195, USA
3Department of Psychosocial and Community Health, University of Washington, Seattle, WA 98195, USA
4Department of Rehabilitation Medicine, University of Washington, Seattle, WA 98195, USA
5Center for Integrative Brain Research, Seattle Children’s Research Institute, Seattle, WA 98101, USA
6Department of Neurology, University of Washington, Seattle, WA 98195, USA

Received 25 June 2014; Accepted 19 October 2014

Academic Editor: Giovanni Li Volti

Copyright © 2015 Kurt E. Weaver et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mitochondrial dysfunction represents a central factor within the pathogenesis of the Alzheimer’s disease (AD) spectrum. We hypothesized that in vivo measurements of lactate (lac), a by-product of glycolysis, would correlate with functional impairment and measures of brain health in a cohort of 15 amnestic mild cognitive impairment (aMCI) individuals. Lac was quantified from the precuneus/posterior cingulate (PPC) using 2-dimensional J-resolved magnetic resonance spectroscopy (MRS). Additionally, standard behavioral and imaging markers of aMCI disease progression were acquired. PPC lac was negatively correlated with performance on the Wechsler logical memory tests and on the minimental state examination even after accounting for gray matter, cerebral spinal fluid volume, and age. No such relationships were observed between lac and performance on nonmemory tests. Significant negative relationships were also noted between PPC lac and hippocampal volume and PPC functional connectivity. Together, these results reveal that aMCI individuals with a greater disease progression have increased concentrations of PPC lac. Because lac is upregulated as a compensatory response to mitochondrial impairment, we propose that J-resolved MRS of lac is a noninvasive, surrogate biomarker of impaired metabolic function and would provide a useful means of tracking mitochondrial function during therapeutic trials targeting brain metabolism.