OBJECTIVE: conventional vascular risk factors (VRFs) are associated with cognitive impairment independent of stroke and detectable cerebral lesions. We used proton magnetic resonance spectroscopy ((1)H MRS) to examine the hypotheses that abnormal levels of brain metabolites may mediate the relationship between VRFs and cognitive impairment. METHODS: a group of 54 stroke-free subjects with various VRFs underwent comprehensive cognitive assessments and (1)H MRS scan of the left hippocampus and prefrontal cortex. We indirectly measured the concentrations of N-acetylaspartate (NAA), choline, inositol, creatine (Cr) and total concentrations of glutamate plus glutamine (Glx). VRFs were quantified by Framingham stroke risk profile (FSRP) score. Subjects were divided into low- (<10%), medium- (10-20%) and high-risk (>20%) groups according to their FSRP scores. Pearson and partial correlation analysis were used to investigate the correlation between FSRP scores and cognitive performance along with the brain metabolism. RESULTS: compared with subjects in low-risk group, high-risk group subjects had significantly poor performances on the tasks of working memory, delayed recall and executive function. In high-risk group, hippocampal Glx/Cr ratios and prefrontal NAA/Cr ratios were significantly lower than those in low-risk group. Lower prefrontal NAA/Cr ratios were associated with executive dysfunction, and lower hippocampal Glx/Cr ratios were associated with impaired delayed recall. CONCLUSION: abnormal concentrations of brain metabolites and decreased glutamate plus glutamine concentration may play an important role in the pathophysiology of VRF-associated cognitive impairment. Brain metabolites detected by (1)H MRS may serve as important markers for monitoring VRFs burden.
OBJECTIVE: conventional vascular risk factors (VRFs) are associated with cognitive impairment independent of stroke and detectable cerebral lesions. We used proton magnetic resonance spectroscopy ((1)H MRS) to examine the hypotheses that abnormal levels of brain metabolites may mediate the relationship between VRFs and cognitive impairment. METHODS: a group of 54 stroke-free subjects with various VRFs underwent comprehensive cognitive assessments and (1)H MRS scan of the left hippocampus and prefrontal cortex. We indirectly measured the concentrations of N-acetylaspartate (NAA), choline, inositol, creatine (Cr) and total concentrations of glutamate plus glutamine (Glx). VRFs were quantified by Framingham stroke risk profile (FSRP) score. Subjects were divided into low- (<10%), medium- (10-20%) and high-risk (>20%) groups according to their FSRP scores. Pearson and partial correlation analysis were used to investigate the correlation between FSRP scores and cognitive performance along with the brain metabolism. RESULTS: compared with subjects in low-risk group, high-risk group subjects had significantly poor performances on the tasks of working memory, delayed recall and executive function. In high-risk group, hippocampal Glx/Cr ratios and prefrontal NAA/Cr ratios were significantly lower than those in low-risk group. Lower prefrontal NAA/Cr ratios were associated with executive dysfunction, and lower hippocampal Glx/Cr ratios were associated with impaired delayed recall. CONCLUSION: abnormal concentrations of brain metabolites and decreased glutamate plus glutamine concentration may play an important role in the pathophysiology of VRF-associated cognitive impairment. Brain metabolites detected by (1)H MRS may serve as important markers for monitoring VRFs burden.