Few MRS studies on aging of the human posterior cingulate cortex have used absolute quantification with correction for CSF content and taken T₂ relaxation into consideration (1-3). Of those, all 3 report higher concentration of total creatine (tCr), 2 report higher choline containing compounds (tCho) and one reports higher N-acetylaspartate (NAA) in the elderly. No differences have been measured in analogous fashion from the occipital cortex (4). The goal of this work was to characterize a larger number of compounds in these brain regions in healthy young and elderly subjects. The key innovation was scanning at ultra-high field (7 T) at very short echo time. Our hypothesis was that higher SNR and spectral dispersion would improve quantification sensitivity and specificity (5) and thus allow us to measure age associated differences in the concentrations of neurochemicals beyond NAA, tCr, and tCho in both regions.Healthy volunteers (Montreal Cognitive Assessment (MoCA) scores ≥ 25), 17 young (age 19-22, 5 subjects scanned 3 times) and 16 elderly (age 70 – 88, 6 subjects scanned 3 times), were studied using a 7-T, 90-cm horizontal bore magnet equipped with a Siemens console and body gradients. A home-built 16-element transmit-receive transmission line head array (6) was used and transmit phase of each channel was optimized via individual 1 kW CPC amplifiers (7). In vivo ¹H NMR spectra were acquired from OCC and PCC volumes of interest (VOI = 8 cm³, figure 1) using a STEAM sequence with VAPOR water suppression and outer volume suppression (8) (TR = 5 s, TE = 8 ms, NA = 64 for OCC, 128 for PCC). First- and second-order shims were adjusted using FASTMAP (9). Metabolite concentrations were quantified using LCModel (10) with a simulated basis set (18 metabolites and experimental macromolecule spectra) and water corrected for tissue content as the internal reference. Only metabolites quantified with Cramer-Rao lower bounds < 35% were included. If the covariance between two metabolites was consistently high (correlation coefficient below -0.7), their sum was reported. Age groups were compared using a 2-tailed t-test with Bonferroni correction for multiple comparisons (p < 0.05/m).Figure 1 illustrates the high quality data achieved in this study in both brain regions and groups studied, and summarizes the findings. Significant differences were observed in a number of metabolites in both brain regions. In the OCC, significantly higher macromolecular content (Mac) and tCho concentration were observed in elderly compared to young. Additionally, the significantly lower concentrations of NAA, N-acetylasparatylglutamate (NAAG), glutamate (Glu), glutathione (GSH), and phosphorylethanolamine (PE) were observed in elderly. In the PCC, higher macromolecular content and higher concentrations of glucose (Glc), myo-inositol (mIns), tCho and tCr and lower concentrations of GABA, Glu, NAA, NAAG and PE were observed in elderly. Using age specific Mac spectra impacted overall quantification.An unprecedented number of differing neurochemical concentrations were measured in the aging human brain. As expected in the elderly, global (i.e., in both brain regions studied) differences in NAA, NAAG, and Glu are consistent with compromised neurons and neurotransmission and differences in tCho and PE are consistent with membrane turnover. Age associated differences in Mac content and composition might be associated with pathological or adaptive processes. More differences were found in the PCC; specifically greater indications of changes in neurotransmission via GABA and inflammation via mIns with additional differences in energy metabolism via tCr and Glc. The only unique difference for the OCC was in the antioxidant GSH. Our outcomes agree with past reports except for the one that found higher tNAA in the PCC (2). Even though it should be most easily detected, neither of the other past reports found an age associated difference for tNAA. A noteworthy difference is that in our study we were able to separate NAA from NAAG.Using high field and a diligent quantification approach, we were able to further support the emerging picture of neuronal loss, gliosis, and inflammation in the aging human brain. The detection of additional neurochemicals bolstered and expanded these concepts and additionally contributed information on energy metabolism and oxidative stress. That some differences were measured in only one of the regions suggests region-specific biochemical aging processes.