Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5735397 | Behavioural Brain Research | 2017 | 6 Pages |
Abstract
Alzheimer's disease (AD) is characterized by neuropathological changes and progressive cognitive decline, which is associated with the volume loss and neurochemical alterations. However, the specific neurochemical alterations in cerebral regions that contribute to cognitive decline still remain unknown. In the present study, we measured cerebral morphological and neurochemical alterations using structural magnetic resonance imaging (MRI) and proton magnetic resonance spectroscopy (1H-MRS) in an AD model of APP/PS1 transgenic mice. Voxel-based morphometry (VBM) analysis indicated atrophy of the hippocampus, motor cortex, striatum, amygdaloid body, septal area, bed nucleus of the stria terminalis and accumbens nucleus in APP/PS1 transgenic mice. Furthermore, the hippocampus was selected as a region of interest (ROI) to explore neurochemical metabolism. The results showed that the ratios of N-acetylaspartate/creatine (NAA/Cr) and glutamate/creatine (Glu/Cr) were reduced, while myo-inositol/creatine (mIn/Cr) was increased in APP/PS1 transgenic mice compared to the wild type mice and accompanied by a decline in learning and memory. Taken together, the present study suggests that hippocampal atrophy and neurochemical changes in NAA, Glu and mIn may play a causative role in the cognitive decline associated with AD.
Keywords
ROIQuantum estimationNaAppmFOVN-acetylaspartate1H-MRSSPM8VBMAdvanced Normalization ToolsMRIRapid Acquisition with Relaxation EnhancementAlzheimer’s diseaseMagnetic resonance imagingQUESTMinecho timeRepetition timeCHESSmagnetic resonance spectroscopyProton magnetic resonance spectroscopyPoint-Resolved Spectroscopyparts per milliongrey matterwhite matterCerebrospinal fluidCSFPRESSregion of interestvoxel-based morphometryAntsMyo-inositolRAREHippocampuscreatineGluglutamate
Related Topics
Life Sciences
Neuroscience
Behavioral Neuroscience
Authors
Shengxiang Liang, Jia Huang, Weilin Liu, Hao Jin, Long Li, Xiufeng Zhang, Binbin Nie, Ruhui Lin, Jing Tao, Shujun Zhao, Baoci Shan, Lidian Chen,