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Differences in grey and white matter atrophy in amnestic mild cognitive impairment and mild Alzheimer's disease
M L F Balthazar1, C L Yasuda, F R Pereira
1Department of Neurology, Medical School, University of Campinas, SP, Brazil.
Background:
Grey matter (GM) atrophy has been demonstrated in amnestic mild cognitive impairment (aMCI) and mild Alzheimer's disease (AD), but the role of white matter (WM) atrophy has not been well characterized. Despite these findings, the validity of aMCI concept as prodromal AD has been questioned.
Methods:
We performed brain MRI with voxel-based morphometry analysis in 48 subjects, aiming to evaluate the patterns of GM and WM atrophy amongst mild AD, aMCI and age-matched normal controls.
Results:
Amnestic mild cognitive impairment GM atrophy was similarly distributed but less intense than that of mild AD group, mainly in thalami and parahippocampal gyri. There were no difference between aMCI and controls concerning WM atrophy. In the mild AD group, we found WM atrophy in periventricular areas, corpus callosum and WM adjacent to associative cortices.
Discussion:
We demonstrated that aMCI might be considered a valid concept to detect very early AD pathology, since we found a close proximity in the pattern of atrophy. Also, we showed the involvement of WM in mild AD, but not in aMCI, suggesting a combination of Wallerian degeneration and microvascular ischaemic disease as a plausible additional pathological mechanism for the discrimination between MCI and AD.
Insights
Amnestic mild cognitive impairment (aMCI) shows grey matter atrophy similar to Alzheimer's disease (AD), but lacks white matter atrophy. This suggests aMCI is an early AD indicator, with white matter changes differentiating MCI from AD.
Area of Science:
- Neuroimaging
- Neurology
- Gerontology
Background:
- Grey matter (GM) atrophy is known in amnestic mild cognitive impairment (aMCI) and Alzheimer's disease (AD).
- The role of white matter (WM) atrophy in aMCI and its relation to AD progression remains unclear.
- The validity of aMCI as a prodromal stage of AD has been questioned.
Purpose of the Study:
- To evaluate patterns of GM and WM atrophy in mild AD, aMCI, and controls.
- To investigate the potential of aMCI as an early indicator of AD pathology.
- To differentiate between aMCI and mild AD based on atrophy patterns.
Main Methods:
- Brain MRI with voxel-based morphometry analysis.
- Comparison of atrophy patterns in 48 subjects across three groups: mild AD, aMCI, and age-matched controls.
Main Results:
- aMCI exhibited GM atrophy in thalami and parahippocampal gyri, similar to but less intense than mild AD.
- No significant WM atrophy was detected in the aMCI group compared to controls.
- Mild AD showed WM atrophy in periventricular areas, corpus callosum, and WM adjacent to associative cortices.
Conclusions:
- The similar pattern of GM atrophy supports aMCI as a valid concept for detecting early AD pathology.
- The absence of WM atrophy in aMCI, contrasted with its presence in mild AD, suggests distinct pathological mechanisms.
- WM involvement in mild AD may involve Wallerian degeneration and microvascular disease, aiding discrimination from MCI.
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