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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

Three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a patient with AD. Lateral (upper) and medial (lower) brain surfaces are shown. Warmer colors indicate higher numbers of plaques and tangles. Adapted and reprinted with permission from Small et al. [16] [Copyright (2008) Lancet Neurology].
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fig3: Three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a patient with AD. Lateral (upper) and medial (lower) brain surfaces are shown. Warmer colors indicate higher numbers of plaques and tangles. Adapted and reprinted with permission from Small et al. [16] [Copyright (2008) Lancet Neurology].

Mentions: Beta-amyloid plaques and neurofibrillary tangles are the two most common neuropathological hallmarks of Alzheimer's disease and they appear in distinctive progressive temporal and spatial patterns of cortical pathology evolution during the disease progression [11]. [F-18]FDDNP is known to bind to amyloid plaques as well as neurofibrillary tangles in vitro [20]. Post mortem neuropathological studies of AD patients who previously received [F-18]FDDNP-PET scans show close matching of in vitro immunohistochemical determined pattern of plaque and tangle distribution in the brain regions with imaging results [16]. [F-18]FDDNP PET-binding patterns of subjects with mild cognitive impairment and AD patients [16] is progressive. Initially increased medial temporal cortex binding in controls at risk and MCI subjects is followed by a variable and progressive pattern of binding in one or more of other cortical areas including posterior cingulate gyrus. In contrast, more advanced AD patients had a pattern of elevated [F-18]FDDNP binding in prefrontal, parietal, posterior cingulate, lateral temporal and medial temporal cortices areas [15, 16, 24]. These results in living humans clearly point at the medial temporal cortex as being the area with the earliest pathological lesion formation which is in accordance with neuropathology findings [11]. Figure 3 shows three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a representative patient with AD.


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)

Three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a patient with AD. Lateral (upper) and medial (lower) brain surfaces are shown. Warmer colors indicate higher numbers of plaques and tangles. Adapted and reprinted with permission from Small et al. [16] [Copyright (2008) Lancet Neurology].
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a patient with AD. Lateral (upper) and medial (lower) brain surfaces are shown. Warmer colors indicate higher numbers of plaques and tangles. Adapted and reprinted with permission from Small et al. [16] [Copyright (2008) Lancet Neurology].
Mentions: Beta-amyloid plaques and neurofibrillary tangles are the two most common neuropathological hallmarks of Alzheimer's disease and they appear in distinctive progressive temporal and spatial patterns of cortical pathology evolution during the disease progression [11]. [F-18]FDDNP is known to bind to amyloid plaques as well as neurofibrillary tangles in vitro [20]. Post mortem neuropathological studies of AD patients who previously received [F-18]FDDNP-PET scans show close matching of in vitro immunohistochemical determined pattern of plaque and tangle distribution in the brain regions with imaging results [16]. [F-18]FDDNP PET-binding patterns of subjects with mild cognitive impairment and AD patients [16] is progressive. Initially increased medial temporal cortex binding in controls at risk and MCI subjects is followed by a variable and progressive pattern of binding in one or more of other cortical areas including posterior cingulate gyrus. In contrast, more advanced AD patients had a pattern of elevated [F-18]FDDNP binding in prefrontal, parietal, posterior cingulate, lateral temporal and medial temporal cortices areas [15, 16, 24]. These results in living humans clearly point at the medial temporal cortex as being the area with the earliest pathological lesion formation which is in accordance with neuropathology findings [11]. Figure 3 shows three-dimensional cortical surface projection images of [F-18]FDDNP-PET scans from a representative patient with AD.

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