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Posterior cingulate GABA and GLX are reduced in amnestic mild cognitive impairment

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Henning,  A       
Research Group MR Spectroscopy and Ultra-High Field Methodology, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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http://www.alzheimersanddementia.com/article/S1552-5260(14)01963-3/pdf
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Citation

Riese, F., Gietl, A., Zölch, N., Henning, A., O'Gorman, R., Kälin, A., et al. (2014). Posterior cingulate GABA and GLX are reduced in amnestic mild cognitive impairment. Poster presented at Alzheimer's Association International Conference (AAIC 2014), Copenhagen, Denmark.


Cite as: https://hdl.handle.net/21.11116/0000-0001-328E-7
Abstract
Background: For preclinical stages of Alzheimer’s disease (AD), the
biomarker potential of in vivo measures of the inhibitory neurotransmitter g -aminobutyric acid (GABA) has not yet been explored.
Methods: We measured GABA, glutamate+glutamine (Glx) and N-acetyl-aspartate (NAA) levels by single-voxel MEGA-PRESS magnetic resonance spectroscopy in the posterior cingulate cortex (PCC) of 22 elderly healthy control subjects (HCS) and 16 age-, gender-, and education-matched patients with amnestic mild cognitive impairment (aMCI). Participants underwent PittsburghCompound B positron emission tomography(PiB-PET), apolipo-protein E (APOE) genotyping, and neuropsychological examination.
Results: In the PCC, GABA, Glx and NAA levels were lower in aMCI pa-
tients. Neurotransmitter levels and NAAwere neither correlated to global or local b -amyloid status nor to APOE genotype, but GABA, Glx, and NAA levelswere positivelycorrelated toverbal learningscores.
Conclusions: Reductions in PCC GABA, Glx and NAA levels may serve as functional biomarkers for cognitive impairment in aMCI. Since they do not seem to reflect amyloid b deposition (or APOE genotype), they are less likely biomarker candidates for preclinical AD.