Abstract
Introduction: While amnestic mild cognitive impairment (aMCI) and non-amnestic mild cognitive impairment (naMCI) are theoretically different entities, only a few investigations studied the structural brain differences between these subtypes of mild cognitive impairment. The aim of the study was to find the structural differences between aMCI and naMCI, and to replicate previous findings on the differentiation between aMCI and healthy controls.Methods: Altogether 62 aMCI, naMCI, and healthy control subjects were included into the study based on the Petersen criteria. All patients underwent a routine brain MR examination, and a detailed neuropsychological examination.Results: The sizes of the hippocampus, the entorhinal cortex and the amygdala were decreased in aMCI relative to naMCI and to controls. Furthermore the cortical thickness of the entorhinal cortex, the fusiform gyrus, the precuneus and the isthmus of the cingulate gyrus were significantly decreased in aMCI relative to naMCI and healthy controls. The largest differences relative to controls were detected for the volume of the hippocampus (18% decrease vs. controls) and the cortical thickness (20% decrease vs. controls) of the entorhinal cortex: 1.6 and 1.4 in terms of Cohen's d. Only the volume of the precuneus were decreased in the naMCI group (5% decrease) compared to the control subjects: 0.9 in terms of Cohen's d. Significant between group differences were also found in the neuropsychological test results: a decreased anterograde, retrograde memory, and category fluency performance was detected in the aMCI group relative to controls and naMCI subjects. Subjects with naMCI showed decreased letter fluency relative to controls, while both MCI groups showed decreased executive functioning relative to controls as measured by the Trail Making test part B. Memory performance in the aMCI group and in the entire sample correlated with the thickness of the entorhinal cortex and with the volume of the amygdala.Conclusion: The amnestic mild cognitive impairment/non-amnestic mild cognitive impairment separation is not only theoretical but backed by structural imaging methods and neuropsychological tests. A better knowledge of the MCI subtypes can help to predict the direction of progression and create targeted prevention.
Highlights
While amnestic mild cognitive impairment and non-amnestic mild cognitive impairment are theoretically different entities, only a few investigations studied the structural brain differences between these subtypes of mild cognitive impairment
Based on previous studies on mild cognitive impairment” (MCI) and conversion to dementia we focused on structures of the temporal lobe and the neighboring regions (Chiang et al, 2011): the entorhinal cortex, the hippocampus, the parahippocampal cortex, the amygdala, the fusiform gyrus, the precuneus, the posterior cingulate cortex, and the isthmus of cingulate gyrus
The post hoc tests showed that the volumes are significantly decreased in the amnestic mild cognitive impairment (aMCI) group relative to the controls and to the non-amnestic mild cognitive impairment (naMCI) group, while the other two groups did not differ significantly (Table 3 and Figure 1) Among the covariates, gender had a significant effect on the volume of the hippocampus, male subjects had a significantly decreased hippocampus size relative to females [F(2, 61) = 7.9, p = 0.007]
Summary
While amnestic mild cognitive impairment (aMCI) and non-amnestic mild cognitive impairment (naMCI) are theoretically different entities, only a few investigations studied the structural brain differences between these subtypes of mild cognitive impairment. The aim of the study was to find the structural differences between aMCI and naMCI, and to replicate previous findings on the differentiation between aMCI and healthy controls. The higher conversion rate to NCD in MCI gives the clinical significance of this pre-disease condition. Conversion rate to NCD is 10–15% annually in MCI compared to the annual rate of 1–4% in the average elderly population (Petersen et al, 2001; Bischkopf et al, 2002).The majority of these patients develop clinical AD. In view of the above it is understandable that several studies target the symptoms and differences from the average population that are closely linked to the development of dementia and can be used to assist the early diagnosis
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