ABORDAGEM E MULTIMODALIDADE DE IMAGEM EM DOENÇA DE ALZHEIMER. PARTE II: ESPECTROSCOPIA, FDG-PET, E IMAGEM AMILÓIDE.

Nesta revisão Parte II, como complemento da revisão Parte I publicada nesta edição, os autores descrevem as técnicas de imagem que avaliam a doença de Alzheimer de acordo com os diferentes perfis metabólicos e moleculares que caracterizam esta doença. Nesta seção são discutidos em profundidade a espectroscopia por ressonância magnética, FDG-PET and imagem com marcadores de peptide beta amilóide.

Palavras-chave:
doença de Alzheimer; demencia; espectroscopia; FDG-PET; e imagem amilóide

Autoria

Chetsadaporn Promteangtrong

Department of Radiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. University of PennsylvaniaUSAPhiladelphia, Pennsylvania, USADepartment of Radiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.

Marcus Kolber

Priya Ramchandra

Mateen Moghbel

Stanford University School of Medicine, Stanford, California. USA Stanford UniversityUSAStanford, California, USAStanford University School of Medicine, Stanford, California. USA

Sina Houshmand

Michael Schöll

Karolinska Institutet, Alzheimer Neurobiology Center, Stockholm, Sweden. Karolinska InstitutetSwedenStockholm, SwedenKarolinska Institutet, Alzheimer Neurobiology Center, Stockholm, Sweden.

Thomas J. Werner

Abass Alavi

Carlos Buchpiguel

Nuclear Medicine Service, Instituto do Cancer do Estado de São Paulo, University of São Paulo, São Paulo, Brazil. University of São PauloBrazilSão Paulo, BrazilNuclear Medicine Service, Instituto do Cancer do Estado de São Paulo, University of São Paulo, São Paulo, Brazil.

Nuclear Medicine Center, Radiology Institute, University of São Paulo General Hospital , São Paulo, Brazil.University of São PauloBrazilSão Paulo, BrazilNuclear Medicine Center, Radiology Institute, University of São Paulo General Hospital , São Paulo, Brazil.

Carlos Alberto Buchpiguel. Av. Arruda Botelho 354 / 14º andar - 05466-000 São Paulo SP - Brazil. E-mail:buch@usp.br

Author contributions. All authors contributed substantially to the preparation and revision of the manuscript

Disclosure: The authors report no conflits of interest

SCIMAGO INSTITUTIONS RANKINGS

Stanford University School of Medicine, Stanford, California. USA Stanford UniversityUSAStanford, California, USAStanford University School of Medicine, Stanford, California. USA

Karolinska Institutet, Alzheimer Neurobiology Center, Stockholm, Sweden. Karolinska InstitutetSwedenStockholm, SwedenKarolinska Institutet, Alzheimer Neurobiology Center, Stockholm, Sweden.

Figuras

Figuras (7)

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Figure 1
1H MR spectroscopy (1H MRS) in the clinical evaluation of a patient with Alzheimer's disease (AD). The graphic at the top is an example of 1H MRS at the posterior cingulate of a normal volunteer. Below, find an example of 1H MRS of a patient with AD. Note the reduction of N-Acetylaspartate (NAA) and increase of myoinositol (mI) peaks.

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Figure 2
FDG-PET of a patient with Alzheimer's disease. Transversal slices show marked hypometabolism in the posterior cingulate cortex and posterior temporoparietal association cortex. Note the difference in glucose metabolism of the posterior portions of the brain compared to the frontal lobes.

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Figure 3
Example of an advanced case of Alzheimer's disease. Note progression of the metabolic posterior temporoparietal impairment towards the frontal lobes, with spared motor and visual cortices activity.

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Figure 4
FDG-PET of a patient with a clinical picture of subtle change in behavior and other cognitive impairments suggestive of frontotemporal dementia (FTD). Note the marked reduced glucose uptake in the frontal lobes and in the anterior portion of the temporal lobes. A suggestive PET finding of FTD.

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Figure 5
Example of PET findings in Lewy Body Dementia. Note marked hypometabolism in parietal and occipital regions of the brain, a distinct pattern from AD.

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Figure 6
Normal amyloid PET example. Note normal uptake of PIB (Pittsburg Compound) labeled with carbon-11 in white matter tissue at the left column. In the middle column it is shown the MR images of the patient, and in the right column the fused images (PIB + MRI). No cortical uptake of 11C-PIB is seen in this case.

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Figure 7
Abnormal PIB PET imaging a patient with confirmed clinical diagnosis of Alzheimer disease. Note marked uptake in the frontal and parietal cortex, with poor visualization of white matter uptake. Right column is the PIB images, middle the MRI and the left column is seen the fused images (PIB + MRI).

Figure 1 1H MR spectroscopy (1H MRS) in the clinical evaluation of a patient with Alzheimer's disease (AD). The graphic at the top is an example of 1H MRS at the posterior cingulate of a normal volunteer. Below, find an example of 1H MRS of a patient with AD. Note the reduction of N-Acetylaspartate (NAA) and increase of myoinositol (mI) peaks.

Figure 2 FDG-PET of a patient with Alzheimer's disease. Transversal slices show marked hypometabolism in the posterior cingulate cortex and posterior temporoparietal association cortex. Note the difference in glucose metabolism of the posterior portions of the brain compared to the frontal lobes.

Figure 3 Example of an advanced case of Alzheimer's disease. Note progression of the metabolic posterior temporoparietal impairment towards the frontal lobes, with spared motor and visual cortices activity.

Figure 4 FDG-PET of a patient with a clinical picture of subtle change in behavior and other cognitive impairments suggestive of frontotemporal dementia (FTD). Note the marked reduced glucose uptake in the frontal lobes and in the anterior portion of the temporal lobes. A suggestive PET finding of FTD.

Figure 5 Example of PET findings in Lewy Body Dementia. Note marked hypometabolism in parietal and occipital regions of the brain, a distinct pattern from AD.

Figure 6 Normal amyloid PET example. Note normal uptake of PIB (Pittsburg Compound) labeled with carbon-11 in white matter tissue at the left column. In the middle column it is shown the MR images of the patient, and in the right column the fused images (PIB + MRI). No cortical uptake of 11C-PIB is seen in this case.

Figure 7 Abnormal PIB PET imaging a patient with confirmed clinical diagnosis of Alzheimer disease. Note marked uptake in the frontal and parietal cortex, with poor visualization of white matter uptake. Right column is the PIB images, middle the MRI and the left column is seen the fused images (PIB + MRI).

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Academia Brasileira de Neurologia, Departamento de Neurologia Cognitiva e Envelhecimento R. Vergueiro, 1353 sl.1404 - Ed. Top Towers Offices, Torre Norte, São Paulo, SP, Brazil, CEP 04101-000, Tel.: +55 11 5084-9463 | +55 11 5083-3876 - São Paulo - SP - Brazil
E-mail: revistadementia@abneuro.org.br | demneuropsy@uol.com.br

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ABORDAGEM E MULTIMODALIDADE DE IMAGEM EM DOENÇA DE ALZHEIMER. PARTE II: ESPECTROSCOPIA, FDG-PET, E IMAGEM AMILÓIDE.

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[1] Carlos Alberto Buchpiguel. Av. Arruda Botelho 354 / 14º andar - 05466-000 São Paulo SP - Brazil. E-mail:buch@usp.br