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Amyloid PET imaging: applications beyond Alzheimer's disease.

Catafau AM, Bullich S - Clin Transl Imaging (2015)

Bottom Line: Besides Alzheimer's disease (AD), deposits of beta-amyloid in the brain are also present in other neurodegenerative diseases associated to dementia, such as Parkinson's disease and dementia with Lewy bodies, as well as in other processes affecting brain function, such as cerebral amyloid angiopathy, brain trauma, Down's syndrome and meningiomas, as shown by post-mortem pathology studies.Furthermore, in systemic amyloidosis other organs besides the brain are affected, and amyloid PET imaging may be suitable for the identification of these extra-cerebral amyloid depositions.Finally, the potential use of amyloid PET tracer accumulation in cerebral white matter (WM) as a marker of myelin is being investigated, leading to some promising results in patients with WM lesions and multiple sclerosis.

View Article: PubMed Central - PubMed

Affiliation: Clinical R&D Neurosciences, Piramal Imaging GmbH, Tegeler Straße 6-7, 13353 Berlin, Germany.

ABSTRACT

As a biomarker of beta-amyloid, positron emission tomography (PET) amyloid imaging offers a unique opportunity to detect the presence of this protein in the human body during life. Besides Alzheimer's disease (AD), deposits of beta-amyloid in the brain are also present in other neurodegenerative diseases associated to dementia, such as Parkinson's disease and dementia with Lewy bodies, as well as in other processes affecting brain function, such as cerebral amyloid angiopathy, brain trauma, Down's syndrome and meningiomas, as shown by post-mortem pathology studies. Furthermore, in systemic amyloidosis other organs besides the brain are affected, and amyloid PET imaging may be suitable for the identification of these extra-cerebral amyloid depositions. Finally, the potential use of amyloid PET tracer accumulation in cerebral white matter (WM) as a marker of myelin is being investigated, leading to some promising results in patients with WM lesions and multiple sclerosis. In this article, a review of the ongoing research pointing to a broader application of amyloid PET imaging in clinical practice beyond AD is provided.

No MeSH data available.


Related in: MedlinePlus

Representative 11C-PIB PET images at two transaxial levels from normal control (NC) (11C-PIB-negative), Alzheimer’s disease (AD), and cerebral amyloid angiopathy (CAA) subjects. Compared with AD and NC, CAA subjects had an intermediate level of global 11C-PIB retention, but compared with AD, had relatively increased occipital retention. Microbleeds seen in this patient, shown in coregistered gradient echo magnetic resonance images, at times appear proximal to foci of amyloid deposition (small arrows). Reproduced from Ann Neurol, Johnson et al. [34] ©2007 with permission from the American Neurological Association
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Fig2: Representative 11C-PIB PET images at two transaxial levels from normal control (NC) (11C-PIB-negative), Alzheimer’s disease (AD), and cerebral amyloid angiopathy (CAA) subjects. Compared with AD and NC, CAA subjects had an intermediate level of global 11C-PIB retention, but compared with AD, had relatively increased occipital retention. Microbleeds seen in this patient, shown in coregistered gradient echo magnetic resonance images, at times appear proximal to foci of amyloid deposition (small arrows). Reproduced from Ann Neurol, Johnson et al. [34] ©2007 with permission from the American Neurological Association

Mentions: Amyloid PET tracer binding to fibrillar amyloid in perivascular beta-amyloid depositions (hallmark of CAA) in addition to beta-amyloid plaques in the cerebral parenchyma (hallmark of AD), has been reported using 11C-PIB [32, 33] which hass been the most extensively used tracer to investigate the potential clinical utility of amyloid imaging in CAA (Table 2). Since the PET signal cannot distinguish between binding in parenchymal beta-amyloid plaques and beta-amyloid in vessel walls, and given the high incidence of CAA in AD patients, the inclusion of non-demented CAA patients in the amyloid PET studies is an indirect way to minimize the effect of accompanying AD pathology [34]. This may explain the lack of significant differences in average cortical 18F-florbetapir SUVR found in one study between AD cases with and without higher CAA density [35], in contrast to the replicated finding of a higher 11C-PIB uptake in non-demented CAA patients, which has been consistently reported to be intermediate between healthy controls and AD [34, 36, 37]. Interestingly, the amyloid accumulation pattern seems to differ from the AD pattern in that the occipital lobe is more frequently affected in CAA (Fig. 2). Quantification may be required to pick up better this different pattern than visual assessment [38], and a higher occipital to global 11C-PIB ratio in CAA than in AD has been a replicated finding [34, 36, 37]. Further in-vivo data supporting the feasibility for the identification on 11C-PIB binding in vascular amyloid include the co-localization of 11C-PIB uptake with MH as detected by magnetic resonance imaging (MRI) [39], the correlation with WM hyperitensities (WMH) volume in probable CAA patients but not in AD or cognitively normal controls [40] and the higher 11C-PIB uptake in cognitively normal controls with lobar MH than in those without lobar MH [41].Table 2


Amyloid PET imaging: applications beyond Alzheimer's disease.

Catafau AM, Bullich S - Clin Transl Imaging (2015)

Representative 11C-PIB PET images at two transaxial levels from normal control (NC) (11C-PIB-negative), Alzheimer’s disease (AD), and cerebral amyloid angiopathy (CAA) subjects. Compared with AD and NC, CAA subjects had an intermediate level of global 11C-PIB retention, but compared with AD, had relatively increased occipital retention. Microbleeds seen in this patient, shown in coregistered gradient echo magnetic resonance images, at times appear proximal to foci of amyloid deposition (small arrows). Reproduced from Ann Neurol, Johnson et al. [34] ©2007 with permission from the American Neurological Association
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4339781&req=5

Fig2: Representative 11C-PIB PET images at two transaxial levels from normal control (NC) (11C-PIB-negative), Alzheimer’s disease (AD), and cerebral amyloid angiopathy (CAA) subjects. Compared with AD and NC, CAA subjects had an intermediate level of global 11C-PIB retention, but compared with AD, had relatively increased occipital retention. Microbleeds seen in this patient, shown in coregistered gradient echo magnetic resonance images, at times appear proximal to foci of amyloid deposition (small arrows). Reproduced from Ann Neurol, Johnson et al. [34] ©2007 with permission from the American Neurological Association
Mentions: Amyloid PET tracer binding to fibrillar amyloid in perivascular beta-amyloid depositions (hallmark of CAA) in addition to beta-amyloid plaques in the cerebral parenchyma (hallmark of AD), has been reported using 11C-PIB [32, 33] which hass been the most extensively used tracer to investigate the potential clinical utility of amyloid imaging in CAA (Table 2). Since the PET signal cannot distinguish between binding in parenchymal beta-amyloid plaques and beta-amyloid in vessel walls, and given the high incidence of CAA in AD patients, the inclusion of non-demented CAA patients in the amyloid PET studies is an indirect way to minimize the effect of accompanying AD pathology [34]. This may explain the lack of significant differences in average cortical 18F-florbetapir SUVR found in one study between AD cases with and without higher CAA density [35], in contrast to the replicated finding of a higher 11C-PIB uptake in non-demented CAA patients, which has been consistently reported to be intermediate between healthy controls and AD [34, 36, 37]. Interestingly, the amyloid accumulation pattern seems to differ from the AD pattern in that the occipital lobe is more frequently affected in CAA (Fig. 2). Quantification may be required to pick up better this different pattern than visual assessment [38], and a higher occipital to global 11C-PIB ratio in CAA than in AD has been a replicated finding [34, 36, 37]. Further in-vivo data supporting the feasibility for the identification on 11C-PIB binding in vascular amyloid include the co-localization of 11C-PIB uptake with MH as detected by magnetic resonance imaging (MRI) [39], the correlation with WM hyperitensities (WMH) volume in probable CAA patients but not in AD or cognitively normal controls [40] and the higher 11C-PIB uptake in cognitively normal controls with lobar MH than in those without lobar MH [41].Table 2

Bottom Line: Besides Alzheimer's disease (AD), deposits of beta-amyloid in the brain are also present in other neurodegenerative diseases associated to dementia, such as Parkinson's disease and dementia with Lewy bodies, as well as in other processes affecting brain function, such as cerebral amyloid angiopathy, brain trauma, Down's syndrome and meningiomas, as shown by post-mortem pathology studies.Furthermore, in systemic amyloidosis other organs besides the brain are affected, and amyloid PET imaging may be suitable for the identification of these extra-cerebral amyloid depositions.Finally, the potential use of amyloid PET tracer accumulation in cerebral white matter (WM) as a marker of myelin is being investigated, leading to some promising results in patients with WM lesions and multiple sclerosis.

View Article: PubMed Central - PubMed

Affiliation: Clinical R&D Neurosciences, Piramal Imaging GmbH, Tegeler Straße 6-7, 13353 Berlin, Germany.

ABSTRACT

As a biomarker of beta-amyloid, positron emission tomography (PET) amyloid imaging offers a unique opportunity to detect the presence of this protein in the human body during life. Besides Alzheimer's disease (AD), deposits of beta-amyloid in the brain are also present in other neurodegenerative diseases associated to dementia, such as Parkinson's disease and dementia with Lewy bodies, as well as in other processes affecting brain function, such as cerebral amyloid angiopathy, brain trauma, Down's syndrome and meningiomas, as shown by post-mortem pathology studies. Furthermore, in systemic amyloidosis other organs besides the brain are affected, and amyloid PET imaging may be suitable for the identification of these extra-cerebral amyloid depositions. Finally, the potential use of amyloid PET tracer accumulation in cerebral white matter (WM) as a marker of myelin is being investigated, leading to some promising results in patients with WM lesions and multiple sclerosis. In this article, a review of the ongoing research pointing to a broader application of amyloid PET imaging in clinical practice beyond AD is provided.

No MeSH data available.


Related in: MedlinePlus