Diffusion tensor imaging of cingulum fibers in mild cognitive impairment and Alzheimer disease

Johns Hopkins University, Baltimore, Maryland, United States
Neurology (Impact Factor: 8.29). 02/2007; 68(1):13-9. DOI: 10.1212/01.wnl.0000250326.77323.01
Source: PubMed


Neuroimaging in mild cognitive impairment (MCI) and Alzheimer disease (AD) generally shows medial temporal lobe atrophy and diminished glucose metabolism and cerebral blood flow in the posterior cingulate gyrus. However, it is unclear whether these abnormalities also impact the cingulum fibers, which connect the medial temporal lobe and the posterior cingulate regions.
To use diffusion tensor imaging (DTI), by measuring fractional anisotropy (FA), to test 1) if MCI and AD are associated with DTI abnormalities in the parahippocampal and posterior cingulate regions of the cingulum fibers; 2) if white matter abnormalities extend to the neocortical fiber connections in the corpus callosum (CC); 3) if DTI improves accuracy to separate AD and MCI from healthy aging vs structural MRI.
DTI and structural MRI were preformed on 17 patients with AD, 17 with MCI, and 18 cognitively normal (CN) subjects.
FA of the cingulum fibers was significantly reduced in MCI, and even more in AD. FA was also significantly reduced in the splenium of the CC in AD, but not in MCI. Adding DTI to hippocampal volume significantly improved the accuracy to separate MCI and AD from CN.
Assessment of the cingulum fibers using diffusion tensor imaging may aid early diagnosis of Alzheimer disease.

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Available from: Susanne G Mueller, May 05, 2014
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    • "Understanding the neural mechanism by which the APOE polymorphism influences WM structure is crucial, particularly because APOE plays a major role in distributing essential lipids that contribute to the development of myelin sheath [20] [21]. Previous DTI studies of older healthy APOE 4 carriers , have found reduced fractional anisotropy (FA) in the splenium of the corpus collosum [22], the cingulum bundle [23] [24], and parahippocampal gyrus [25]. A recent study into younger APOE 4 carriers reported non-significant differences in WM structure, but found subtle differences within the prefrontal cortex between carriers and non-carriers [26]. "
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    ABSTRACT: The apolipoprotein E (APOE) ɛ4 allele is the best established genetic risk factor for Alzheimer's disease (AD) and has been previously associated with alterations in structural gray matter and changes in functional brain activity in healthy middle-aged individuals and older non-demented subjects. In order to determine the neural mechanism by which APOE polymorphisms affect white matter (WM) structure, we investigated the diffusion characteristics of WM tracts in carriers and non-carriers of the APOE ɛ4 and ɛ2 alleles using an unbiased whole brain analysis technique (Tract Based Spatial Statistics) in a healthy young adolescent (14 years) cohort. A large sample of healthy young adolescents (n = 575) were selected from the European neuroimaging-genetics IMAGEN study with available APOE status and accompanying diffusion imaging data. MR Diffusion data was acquired on 3T systems using 32 diffusion-weighted (DW) directions and 4 non-DW volumes (b-value = 1,300 s/mm2 and isotropic resolution of 2.4×2.4×2.4 mm). No significant differences in WM structure were found in diffusion indices between carriers and non-carriers of the APOE ɛ4 and ɛ2 alleles, and dose-dependent effects of these variants were not established, suggesting that differences in WM structure are not modulated by the APOE polymorphism. In conclusion, our results suggest that microstructural properties of WM structure are not associated with the APOE ɛ4 and ɛ2 alleles in young adolescence, suggesting that the neural effects of these variants are not evident in 14-year-olds and may only develop later in life.
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    • "Instead, we smoothed the image with a 2 mm kernel using FSLMATHS. To protect against Type I error we identified tracts previously reported to be associated with AD (Fig. 1) and divided them by hemisphere: the cingulum (CCG) (Xie et al. 2005; Zhang et al. 2007, 2014; Burzynska et al. 2010; Liu et al. 2011), the inferior fronto-occipital fasciculus (IFOF) (Gold et al. 2010; Teipel et al. 2010; Alves et al. 2012), the superior longitudinal fasciculus (SLF) (Liu et al. 2011; Sexton et al. 2011; Alves et al. 2012; Bosch et al. 2012), and the uncinate fasciculus (UF) (Liu et al. 2011; Sexton et al. 2011; Bosch et al. 2012). We created our white matter binary tract masks from the Johns Hopkins University (JHU) probabilistic atlas registered to the common MNI space (Mori et al. 2005; Hua et al. 2008). "
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    • "Still, our results may provide a few clues to start deciphering these pathways. First, the strong relation of the MeDi with WM microstructure in extensive areas (with no specific involvement of tracts generally altered in AD, e.g., the cingulum and fornix) along with the absence of meaningful association with GM atrophy (specifically in AD regions, e.g., the hippocampus) suggests that mechanisms are not primarily related to AD neurodegeneration [35] [36] [37] [38] [39] [40]. It remains possible that our study was underpowered to detect associations with volumes; however, we were able to detect the effect of age, suggesting sufficient power in this sample to capture wellestablished risk factors for brain atrophy. "
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