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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

Surface maps indicating the pattern of [C-11]PIB binding obtained with 10 patients with clinical Alzheimer's disease compared with 29 healthy older control subjects. Adapted and reprinted with permission from Buckner et al. [21] [Copyright (2005) Journal of Neuroscience].
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Related In: Results  -  Collection


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fig4: Surface maps indicating the pattern of [C-11]PIB binding obtained with 10 patients with clinical Alzheimer's disease compared with 29 healthy older control subjects. Adapted and reprinted with permission from Buckner et al. [21] [Copyright (2005) Journal of Neuroscience].

Mentions: PET imaging studies with [C-11]PIB, which has been suggested to bind to amyloid plaques only [40, 41], show a single pattern of [C-11]PIB binding in the prefrontal, lateral parietal, posterior cingulate, lateral temporal cortices and precuneus [40] at all levels of cognitive impairment, including AD, a subset of MCI subjects and even some cognitively normal controls. This pattern of [C-11]PIB cortical uptake was correlated with the DMN by Buckner et al. [21] who noticed overlap of DMN and [C-11]PIB-binding pattern in cortical areas with exception of the medial temporal cortex which include both hippocampus and parahippocampal gyrus (see Figure 4). When compared with the patterns of known beta-amyloid deposition in AD [11, 42, 43], this lack of [C-11]PIB binding in the hippocampus and neocortical areas of medial temporal cortex (entorhinal, parahippocampal, rhinal, and perirhinal cortices) points to the most significant mismatch between beta-amyloid pathology and [C-11]PIB binding. Indeed multiple contradictory [C-11]PIB-binding results in humans have been reported [44] and recent work demonstrating that [C-11]PIB brain accumulation may be at least in part mediated by [C-11]PIB sulfation via estrogen sulfotransferase [45] has cast doubts on the purported human amyloid specificity of [C-11]PIB.


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)

Surface maps indicating the pattern of [C-11]PIB binding obtained with 10 patients with clinical Alzheimer's disease compared with 29 healthy older control subjects. Adapted and reprinted with permission from Buckner et al. [21] [Copyright (2005) Journal of Neuroscience].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Surface maps indicating the pattern of [C-11]PIB binding obtained with 10 patients with clinical Alzheimer's disease compared with 29 healthy older control subjects. Adapted and reprinted with permission from Buckner et al. [21] [Copyright (2005) Journal of Neuroscience].
Mentions: PET imaging studies with [C-11]PIB, which has been suggested to bind to amyloid plaques only [40, 41], show a single pattern of [C-11]PIB binding in the prefrontal, lateral parietal, posterior cingulate, lateral temporal cortices and precuneus [40] at all levels of cognitive impairment, including AD, a subset of MCI subjects and even some cognitively normal controls. This pattern of [C-11]PIB cortical uptake was correlated with the DMN by Buckner et al. [21] who noticed overlap of DMN and [C-11]PIB-binding pattern in cortical areas with exception of the medial temporal cortex which include both hippocampus and parahippocampal gyrus (see Figure 4). When compared with the patterns of known beta-amyloid deposition in AD [11, 42, 43], this lack of [C-11]PIB binding in the hippocampus and neocortical areas of medial temporal cortex (entorhinal, parahippocampal, rhinal, and perirhinal cortices) points to the most significant mismatch between beta-amyloid pathology and [C-11]PIB binding. Indeed multiple contradictory [C-11]PIB-binding results in humans have been reported [44] and recent work demonstrating that [C-11]PIB brain accumulation may be at least in part mediated by [C-11]PIB sulfation via estrogen sulfotransferase [45] has cast doubts on the purported human amyloid specificity of [C-11]PIB.

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