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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

Comparison of [C-11]PIB SPM t-map image (red) and [F-18]FDDNP SPM t-map image (green) obtained with 10 AD patients compared with 10 healthy age-matched control subjects (P < .05, uncorrected, k = 100). The yellow area represents the area where the [C-11]PIB SPM t-map (red) and [F-18]FDDNP SPM t-map (green) overlapped. Adapted and reprinted with permission from Shin et al. [25] [Copyright (2010) Neuroimage].
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fig5: Comparison of [C-11]PIB SPM t-map image (red) and [F-18]FDDNP SPM t-map image (green) obtained with 10 AD patients compared with 10 healthy age-matched control subjects (P < .05, uncorrected, k = 100). The yellow area represents the area where the [C-11]PIB SPM t-map (red) and [F-18]FDDNP SPM t-map (green) overlapped. Adapted and reprinted with permission from Shin et al. [25] [Copyright (2010) Neuroimage].

Mentions: It may be possible that other factors, like cortical atrophy and/or low distribution of amyloid aggregates may contribute to the underestimation of [C-11]PIB accumulation in medial temporal lobe (MTL). Indeed, topographical differences in the distribution of senile plaques (SP) and neurofibrillary tangles (NFT) have been noted in AD, with lower densities of SP in limbic areas of MTL, such as hippocampus and subiculum, which are more affected by neurofibrillary tangle pathology [10]. Yet in other areas of medial temporal lobe, such as entorhinal, perirhinal, and rhinal cortices as well as parahippocampal gyrus, β-amyloid plaque densities (both diffuse and neuritic plaques) reach levels observed in lateral temporal lobe and other cortical areas even in subjects without clinically manifested dementia and only limited atrophy [43]. Thus, even though some partial volume effects are expected, it is unlikely that [C-11]PIB negligible binding in MTL at all levels of cognitive impairment is entirely due to the combined effects of low β-amyloid plaque densities and atrophy. If so, one would also expect a similar drastic effect of MTL atrophy with the [F-18]FDDNP signal in the same patients, and this is not observed (Figures 5 and 6).


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)

Comparison of [C-11]PIB SPM t-map image (red) and [F-18]FDDNP SPM t-map image (green) obtained with 10 AD patients compared with 10 healthy age-matched control subjects (P < .05, uncorrected, k = 100). The yellow area represents the area where the [C-11]PIB SPM t-map (red) and [F-18]FDDNP SPM t-map (green) overlapped. Adapted and reprinted with permission from Shin et al. [25] [Copyright (2010) Neuroimage].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: Comparison of [C-11]PIB SPM t-map image (red) and [F-18]FDDNP SPM t-map image (green) obtained with 10 AD patients compared with 10 healthy age-matched control subjects (P < .05, uncorrected, k = 100). The yellow area represents the area where the [C-11]PIB SPM t-map (red) and [F-18]FDDNP SPM t-map (green) overlapped. Adapted and reprinted with permission from Shin et al. [25] [Copyright (2010) Neuroimage].
Mentions: It may be possible that other factors, like cortical atrophy and/or low distribution of amyloid aggregates may contribute to the underestimation of [C-11]PIB accumulation in medial temporal lobe (MTL). Indeed, topographical differences in the distribution of senile plaques (SP) and neurofibrillary tangles (NFT) have been noted in AD, with lower densities of SP in limbic areas of MTL, such as hippocampus and subiculum, which are more affected by neurofibrillary tangle pathology [10]. Yet in other areas of medial temporal lobe, such as entorhinal, perirhinal, and rhinal cortices as well as parahippocampal gyrus, β-amyloid plaque densities (both diffuse and neuritic plaques) reach levels observed in lateral temporal lobe and other cortical areas even in subjects without clinically manifested dementia and only limited atrophy [43]. Thus, even though some partial volume effects are expected, it is unlikely that [C-11]PIB negligible binding in MTL at all levels of cognitive impairment is entirely due to the combined effects of low β-amyloid plaque densities and atrophy. If so, one would also expect a similar drastic effect of MTL atrophy with the [F-18]FDDNP signal in the same patients, and this is not observed (Figures 5 and 6).

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