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Brain biomarkers derived by proton magnetic resonance spectroscopy may indicate brain energetic changes in Alzheimer’s disease (643.12)
Author(s) -
Taylor Matthew,
Swerdlow Russell,
Vidoni Eric,
Morris Jill,
Sullivan Debra,
Burns Jeffrey
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.643.12
Subject(s) - white matter , creatine , medicine , glutamine , magnetic resonance imaging , glutamate receptor , endocrinology , pathology , chemistry , biochemistry , radiology , receptor , amino acid
BACKGROUND: Metabolic changes in the brain have been proposed to lend to Alzheimer’s disease (AD) etiology. Proton Magnetic resonance spectroscopy (MRS) allows in‐vivo measurement of brain metabolites that have been implicated in brain energy metabolism. METHODS: 120 subjects 蠅65 years old (58 non‐demented, CDR 0; 50 very mild AD, CDR 0.5; and 12 mild AD, CDR 1.0) were included in this cross‐sectional study. Brain concentrations of n‐acetyl aspartate (NAA), myoinositol (MI), glutamate+glutamine (Glu+Gln) and creatine (Cr) were measured in 6 different brain regions via MRS. ANOVA was performed using CDR 0 as the control. RESULTS: MI was elevated in posterior gray matter in both AD groups (p=.01, p=.05) and elevated exclusively in CDR 0.5 in left frontal white matter (p=.04) and right frontal white matter (p=.04). NAA was reduced in CDR 0.5 left frontal white matter (p=.05) and left temporal white matter (p=.04) and reduced in CDR 1.0 expressed as NAA/Cr in posterior gray matter (p=.01). Glu+Gln/Cr was reduced in in both AD groups in posterior gray matter (p=.04, p=.01) and right temporal white matter (p=.04, p=.02) and in left frontal white matter (p=.02) in CDR 0.5. DISCUSSION: Biomarkers measured by MRS suggest differences in brain metabolism in AD compared to non‐demented aging. Causality of these changes and their consequence in AD is unknown. It is desirable to know whether diet or therapy could play a role in normalizing biomarker concentrations and offer benefit in AD.