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Multimodal Imaging of Alzheimer Pathophysiology in the Brain's Default Mode Network.

Shin J, Kepe V, Small GW, Phelps ME, Barrio JR - Int J Alzheimers Dis (2011)

Bottom Line: The spatial correlations between the brain's default mode network (DMN) and the brain regions known to develop pathophysiology in Alzheimer's disease (AD) have recently attracted much attention.In this paper, we compare results of different functional and structural imaging modalities, including MRI and PET, and highlight different patterns of anomalies observed within the DMN.Multitracer PET imaging in subjects with and without dementia has demonstrated that [C-11]PIB- and [F-18]FDDNP-binding patterns in patients with AD overlap within nodes of the brain's default network including the prefrontal, lateral parietal, lateral temporal, and posterior cingulate cortices, with the exception of the medial temporal cortex (especially, the hippocampus) where significant discrepancy between increased [F-18]FDDNP binding and negligible [C-11]PIB-binding was observed. [F-18]FDDNP binding in the medial temporal cortex-a key constituent of the DMN-coincides with both the presence of amyloid and tau pathology, and also with cortical areas with maximal atrophy as demonstrated by T1-weighted MR imaging of AD patients.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Institute, Gachon University of Medicine and Science, Incheon 405-760, Republic of Korea.

ABSTRACT
The spatial correlations between the brain's default mode network (DMN) and the brain regions known to develop pathophysiology in Alzheimer's disease (AD) have recently attracted much attention. In this paper, we compare results of different functional and structural imaging modalities, including MRI and PET, and highlight different patterns of anomalies observed within the DMN. Multitracer PET imaging in subjects with and without dementia has demonstrated that [C-11]PIB- and [F-18]FDDNP-binding patterns in patients with AD overlap within nodes of the brain's default network including the prefrontal, lateral parietal, lateral temporal, and posterior cingulate cortices, with the exception of the medial temporal cortex (especially, the hippocampus) where significant discrepancy between increased [F-18]FDDNP binding and negligible [C-11]PIB-binding was observed. [F-18]FDDNP binding in the medial temporal cortex-a key constituent of the DMN-coincides with both the presence of amyloid and tau pathology, and also with cortical areas with maximal atrophy as demonstrated by T1-weighted MR imaging of AD patients.

No MeSH data available.


Related in: MedlinePlus

Patterns of grey matter atrophy in patients with AD compared with age-matched control group. The results are shown on a 3D surface render (top) and overlaid on representative axial, coronal and sagittal slices (bottom). L: left; R: right. Adapted and reprinted with permission from Whitwell et al. [18] [Copyright (2005) Brain].
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Related In: Results  -  Collection


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fig2: Patterns of grey matter atrophy in patients with AD compared with age-matched control group. The results are shown on a 3D surface render (top) and overlaid on representative axial, coronal and sagittal slices (bottom). L: left; R: right. Adapted and reprinted with permission from Whitwell et al. [18] [Copyright (2005) Brain].

Mentions: A variety of pathological processes including neuronal loss, synaptic loss, and loss of projections contribute to gray matter atrophy which spreads across the brain in AD with the disease progression disrupting neuronal circuits involved in the DMN prominently including the medial temporal cortex [17, 21, 22, 34, 35]. The temporal trajectory of cortical atrophy was studied by Whitwell et al. [18] in a longitudinal MRI study of atrophy in amnestic MCI (aMCI) subjects who progressed to AD. The initial pattern of grey matter loss in the aMCI subject scans 3 years prior to the diagnosis of AD was focused primarily in the medial temporal cortex, including the amygdala, anterior hippocampus and entorhinal cortex, with some additional involvement of the fusiform gyrus,. The extent and magnitude of cerebral atrophy in these patients further progressed over the following two years with atrophy in the medial temporal cortex spreading to middle temporal gyrus, and extended into more posterior regions of the temporal cortex to include the entire extent of the hippocampus and partial involvement of the parietal cortex. By the time the subjects had progressed to a clinical diagnosis of AD the pattern of grey matter atrophy had become more widespread with more severe involvement of the medial temporal cortex and the temporoparietal association cortices and, for the first time, substantial involvement of the frontal cortex (see Figure 2).


Multimodal Imaging of Alzheimer Pathophysiology in the Brain's Default Mode Network.

Shin J, Kepe V, Small GW, Phelps ME, Barrio JR - Int J Alzheimers Dis (2011)

Patterns of grey matter atrophy in patients with AD compared with age-matched control group. The results are shown on a 3D surface render (top) and overlaid on representative axial, coronal and sagittal slices (bottom). L: left; R: right. Adapted and reprinted with permission from Whitwell et al. [18] [Copyright (2005) Brain].
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3100676&req=5

fig2: Patterns of grey matter atrophy in patients with AD compared with age-matched control group. The results are shown on a 3D surface render (top) and overlaid on representative axial, coronal and sagittal slices (bottom). L: left; R: right. Adapted and reprinted with permission from Whitwell et al. [18] [Copyright (2005) Brain].
Mentions: A variety of pathological processes including neuronal loss, synaptic loss, and loss of projections contribute to gray matter atrophy which spreads across the brain in AD with the disease progression disrupting neuronal circuits involved in the DMN prominently including the medial temporal cortex [17, 21, 22, 34, 35]. The temporal trajectory of cortical atrophy was studied by Whitwell et al. [18] in a longitudinal MRI study of atrophy in amnestic MCI (aMCI) subjects who progressed to AD. The initial pattern of grey matter loss in the aMCI subject scans 3 years prior to the diagnosis of AD was focused primarily in the medial temporal cortex, including the amygdala, anterior hippocampus and entorhinal cortex, with some additional involvement of the fusiform gyrus,. The extent and magnitude of cerebral atrophy in these patients further progressed over the following two years with atrophy in the medial temporal cortex spreading to middle temporal gyrus, and extended into more posterior regions of the temporal cortex to include the entire extent of the hippocampus and partial involvement of the parietal cortex. By the time the subjects had progressed to a clinical diagnosis of AD the pattern of grey matter atrophy had become more widespread with more severe involvement of the medial temporal cortex and the temporoparietal association cortices and, for the first time, substantial involvement of the frontal cortex (see Figure 2).

Bottom Line: The spatial correlations between the brain's default mode network (DMN) and the brain regions known to develop pathophysiology in Alzheimer's disease (AD) have recently attracted much attention.In this paper, we compare results of different functional and structural imaging modalities, including MRI and PET, and highlight different patterns of anomalies observed within the DMN.Multitracer PET imaging in subjects with and without dementia has demonstrated that [C-11]PIB- and [F-18]FDDNP-binding patterns in patients with AD overlap within nodes of the brain's default network including the prefrontal, lateral parietal, lateral temporal, and posterior cingulate cortices, with the exception of the medial temporal cortex (especially, the hippocampus) where significant discrepancy between increased [F-18]FDDNP binding and negligible [C-11]PIB-binding was observed. [F-18]FDDNP binding in the medial temporal cortex-a key constituent of the DMN-coincides with both the presence of amyloid and tau pathology, and also with cortical areas with maximal atrophy as demonstrated by T1-weighted MR imaging of AD patients.

View Article: PubMed Central - PubMed

Affiliation: Neuroscience Research Institute, Gachon University of Medicine and Science, Incheon 405-760, Republic of Korea.

ABSTRACT
The spatial correlations between the brain's default mode network (DMN) and the brain regions known to develop pathophysiology in Alzheimer's disease (AD) have recently attracted much attention. In this paper, we compare results of different functional and structural imaging modalities, including MRI and PET, and highlight different patterns of anomalies observed within the DMN. Multitracer PET imaging in subjects with and without dementia has demonstrated that [C-11]PIB- and [F-18]FDDNP-binding patterns in patients with AD overlap within nodes of the brain's default network including the prefrontal, lateral parietal, lateral temporal, and posterior cingulate cortices, with the exception of the medial temporal cortex (especially, the hippocampus) where significant discrepancy between increased [F-18]FDDNP binding and negligible [C-11]PIB-binding was observed. [F-18]FDDNP binding in the medial temporal cortex-a key constituent of the DMN-coincides with both the presence of amyloid and tau pathology, and also with cortical areas with maximal atrophy as demonstrated by T1-weighted MR imaging of AD patients.

No MeSH data available.


Related in: MedlinePlus