3D maps from multiple MRI illustrate changing atrophy patterns as subjects progress from mild cognitive impairment to Alzheimer's disease.

By Jennifer L. Whitwell, S. Przybelski, S. Weigand, David S. Knopman, Brad Boeve, Ronald C. Petersen, Clifford R. Jack Jr.. Brain : a journal of neurology, 2007

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Mild cognitive impairment (MCI), particularly the amnestic subtype (aMCI), is considered as a transitional stage between normal aging and a diagnosis of clinically probable Alzheimer's disease (AD). The aMCI construct is particularly useful as it provides an opportunity to assess a clinical stage which in most subjects represents prodromal AD. The aim of this study was to assess the progression of cerebral atrophy over multiple serial MRI during the period from aMCI to progression to AD. Thirty-three subjects were selected that fulfilled clinical criteria for aMCI and had three serial MRI scans: the first scan approximately 3 years before the diagnosis of AD, the second scan approximately 1 year before, and the third scan at the time of the diagnosis of AD. A group of 33 healthy controls were age and gender-matched to the study cohort. Voxel-based morphometry (VBM) was used to assess patterns of grey matter atrophy in the aMCI subjects at each time-point compared to the control group. Customized templates and prior probability maps were used to avoid normalization and segmentation bias. The pattern of grey matter loss in the aMCI subject scans that were 3 years before the diagnosis of AD was focused primarily on the medial temporal lobes, including the amygdala, anterior hippocampus and entorhinal cortex, with some additional involvement of the fusiform gyrus, compared to controls. The extent and magnitude of the cerebral atrophy further progressed by the time the subjects were 1 year before the diagnosis of AD. At this point atrophy in the temporal lobes spread to include the middle temporal gyrus, and extended into more posterior regions of the temporal lobe to include the entire extent of the hippocampus. The parietal lobe also started to become involved. By the time the subjects had progressed to a clinical diagnosis of AD the pattern of grey matter atrophy had become still more widespread with more severe involvement of the medial temporal lobes and the temporoparietal association cortices and, for the first time, substantial involvement of the frontal lobes. This pattern of progression fits well with the Braak and Braak neurofibrillary pathological staging scheme in AD. It suggests that the earliest changes occur in the anterior medial temporal lobe and fusiform gyrus, and that these changes occur at least 3 years before progression to the diagnosis of AD. These results also suggest that 3D patterns of grey matter atrophy may help to predict the time to the first diagnosis of AD in subjects with aMCI.

Subfields: Neurology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/7c2478c24644a22876656ccb80cb8f9d379f6d52

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Citations in the corpus

Automatic classification of patients with Alzheimer's disease from structural MRI: A comparison of ten methods using the ADNI database (2011, background): “…al., 2003; Rusinek et al., 2004; Tapiola et al., 2008), the posterior cingulate gyrus (Karas et al., 2004; Chételat et al., 2005; Laakso et al., 1998) and the posterior middle frontal gyrus (Whitwell et al., 2007), the fusiform gyrus, the thalamus (Karas et al., 2003, 2004; Chételat et al., 2005).”
Harmonization of large MRI datasets for the analysis of brain imaging patterns throughout the lifespan (2019, unknown): “, 2016), that could be linked to age-related pathologies such as neurodegenerative disorders (Dickerson et al., 2009; Whitwell et al., 2007), but also to the normal process of aging, which was suggested to be accompanied by demyelination in the white matter and axonal loss (Hinman and Abraham, 2007)”
Impairment and compensation coexist in amnestic MCI default mode network (2010, unknown): “With the application of voxel based morphology (VBM), measurements of the cerebral gray matter could predict conversion from MCI to AD (Bozzali et al., 2006; Whitwell et al., 2007).”
Spatial patterns of brain atrophy in MCI patients, identified via high-dimensional pattern classification, predict subsequent cognitive decline (2008, methodology): “…2001; Du et al., 2001; Grundman et al., 2002; Chetelat, 2003; Karas et al., 2004; Pennanen et al., 2005; Bozzali et al., 2006; Saykin et al., 2006; Whitwell et al., 2007), the present study finds that brain atrophy in this cohort is already quite extensive and involves superior, middle, and…”
Predictive Markers for AD in a Multi-Modality Framework: An Analysis of MCI Progression in the ADNI Population (2010, background): “A signi ﬁ cant body of existing literature (Johnson et al., 2006; Whitwell et al., 2007; Reiman et al., 1996; Canu et al., 2010; Thompson and Apostolova, 2007) suggests that pathological manifestations of Alzheimer's disease begin many years before the patient becomes symptomatic — which is…”
Aging hippocampus and amygdala (2008, methodology): “For example, using volumetric methods, greater anterior than posterior hippocampal atrophy has been demonstrated in mild cognitive impairment before progression to Alzheimer’s disease [10], in established Alzheimer’s disease [2] and Parkinson’s disease [11].”
Loss of ‘Small-World’ Networks in Alzheimer's Disease: Graph Analysis of fMRI Resting-State Functional Connectivity (2010, background): “Atrophy is a major factor in Alzheimer disease, and its brain distribution and correlation to cognitive decline are well described [64,70,71].”
Structural and functional biomarkers of prodromal Alzheimer's disease: A high-dimensional pattern classification study (2008, background): “…have confirmed that complex spatial patterns of brain atrophy can be measured in MCI and AD (Bozzali et al., 2006; Chetelat et al., 2002; Davatzikos et al., 2008; Karas et al., 2004; Pennanen et al., 2005a; Saykin et al., 2006; Thompson et al., 2001; Whitwell et al., 2007; Xie et al., 2006).”
Hypothetical model of dynamic biomarkers of the Alzheimer’s pathological cascade (2010, unknown): “96 Therefore, at a given timepoint, different brain areas will be at different stages.”