¹ H MR spectroscopy in common dementias

Abstract

Objective-To determine the 1 H MR spectroscopic (MRS) findings and inter-group differences among common dementias: Alzheimer's disease (AD), vascular dementia (VaD), dementia with Lewy bodies (DLB), and frontotemporal lobar degeneration (FTLD).Methods-We consecutively recruited 206 normal elderly, 121 patients with AD, 41 with FTLD, 20 with DLB, and 8 with VaD. We evaluated the 1 H MRS metabolite ratio changes in common dementias with respect to normal, and also differences among the common dementias.Results-N-acetylaspartate/Creatine (NAA/Cr) was lower than normal in patients with AD, FTLD, and VaD. Myo-inositol (mI)/Cr was higher than normal in patients with AD and FTLD. Choline (Cho)/Cr was higher than normal in patients with, AD, FTLD, and DLB. There were no metabolite differences between patients with AD and FTLD, nor between patients with DLB and VaD. NAA / Cr was lower in patients with AD and FTLD than DLB. MI /Cr was higher in patients with AD and FTLD than VaD. MI /Cr was also higher in patients with FTLD than DLB.Conclusions-NAA/Cr levels are decreased in dementias that are characterized by neuron loss such as AD, FTLD, and VaD. MI/Cr levels are elevated in dementias that are pathologically characterized by gliosis such as AD and FTLD. Cho/Cr levels are elevated in dementias that are characterized by a profound cholinergic deficit such as AD and DLB.

Imaging correlates of posterior cortical atrophy

“…The trend of higher mI /Cr levels in PCA compared to AD further suggests a more prominent glial activation in the medial parietal lobes of PCA than AD patients. Furthermore, elevation of the membrane marker Cho /Cr levels in both AD and PCA may indicate increased membrane turnover because of the degenerative process, cholinergic deficit, or both [29].…”

“…An eight cm 3 midline parietal (2×2×2 cm) voxel was placed on a mid-sagittal T1-weighted image including right and left posterior cingulate gyri and inferior precunei [29]. Point resolved spectroscopy (PRESS) pulse sequence with TR = 2000 ms, TE=30 ms, 2048 data points and 128 excitations were used for the examinations.…”

“…A number of VBM studies have demonstrated atrophy of the hippocampus and medial temporal lobe regions, the posterior cingulate gyrus, precuneus, temporoparietal neocortex and prefrontal cortex in typical AD [3,10,30,44,52]. Proton MR spectroscopy ( 1 H MRS) is a technique that provides information regarding the neurochemistry of the brain, and has been useful in differentiating the common degenerative dementias [14,29]. The neuronal integrity marker N-acetyl aspartate (NAA) level is decreased, and the glial activity marker myo-inositol (mI) level is elevated in brain regions affected by the neurodegenerative pathologies in AD and frontotemporal lobar degeneration [14,28].…”

Recent Advances in Magnetic Resonance Neurospectroscopy

“…171,172 These patterns of spectral alterations can be used to differentiate patients with suspected AD from normal elderly controls, as well as patients with other kinds of dementias. 174 These patterns, adapted from Kantarci et al, 174 are summarized in TABLE 1. These data were collected using a short echo PRESS sequence from a voxel positioned in the posterior cingulate gyri and inferior precunei.…”

Proton Magnetic Resonance Spectroscopic Evidence of Glial Effects of Cumulative Lead Exposure in the Adult Human Hippocampus

“…Elevated mI and decreased NAA have been widely reported in patients with Alzheimer disease compared with normal controls in neocortical, limbic cortical, and hippocampal regions (Ross et al 2006). Although other dementias share the feature of a decrease in NAA/Cr, the increase in mI/Cr is a relatively distinctive aspect of Alzheimer disease and has been suggested as indicative of gliosis (Kantarci et al 2004;Ross et al 2006). It has been proposed that the initial MRS changes in the pathologic progression of Alzheimer disease is an increase in mI/Cr and that a decrease in NAA/Cr develops later in the disease course, based on data from the posterior cingulate gyrus (Kantarci et al 2000).…”