The anatomical and functional changes in the primary olfactory cortex of Alzheimer disease and mild cognitive impairment patients / 中华放射学杂志

ABSTRACT

Objective To determine the volume reduction of the primary olfactory cortex (POC) in patients with Alzheimer disease (AD) and investigate the potential relationship of functional olfactory activation and anatomical atrophy changes. Methods Twelve patients with AD, eight patients with mild cognitive impairment (MCI) and twenty normal controls (NC) underwent standardized UPSIT (University of Pennsylvania smell identification test) behavior smell test and neuropsychological tests. Then all of the subjects underwent the high resolution MRI and an olfactory fMRI scan on a 3T system. Volumetric measurement of the POC was conducted and the areas were also saved as a ROI which would be used during the processing of fMRI data to get the activation voxels in local region. The Kruskal-Wallis rank test was used to examine the significance of POC volume and activation in three groups, If P-value was less than 0.05,Bonferroni method was used for multiple comparisons. The correlation between the anatomical volume and functional activation was analyzed with partial correlation adjusted for age. Results The POC volume of NC, MCI and AD groups were 3024--4734, 1409--4553 and 1561--3759 mm~3, and the medians were 3749, 2752 and 2156 mm~3. The activation voxels of each group were 0--2360, 0--2160 and 0--100 mm~3, while the medians were 430, 40 and 0 mm~3. There were significant differences of both POC volume atrophy and activation between the three groups, with a trend of reduction from NC to MCI to AD group (H is 14.942 and 16.587, both P<0.05). The volume of olfactory activation at POC was highly correlated with the volume of POC (r=0.364, P=0.023). Conclusions In this study, we explored the morphological and functional changes in the POC. It is revealed that POC suffers prominent local atrophy and dysfunction as well as hippocampus in AD. These results can provide neuropathological and neurofunctional bases for olfactory deficit in Alzheimer Disease.