Positron Emission Tomography Diagnosis of Alzheimer's Disease

Department of Radiology, Duke University Medical Center, Box 3949, Durham, NC 27710, USA.
Neuroimaging Clinics of North America (Impact Factor: 1.53). 12/2005; 15(4):837-46, x. DOI: 10.1016/j.nic.2005.09.007
Source: PubMed


Positron emission tomography (PET) imaging of [18F]-2-fluoro-2-deoxy-D-glucose (FDG) is accurate in the early detection of Alzheimer's disease (AD) and in the differentiation of AD from the other causes of dementia. FDG-PET imaging is available widely and performed easily. Different patterns of abnormality with the various causes of dementia are well described. Semiquantitative methods of image interpretation are available. Medicare covers FDG-PET imaging for the narrow indication of differentiation of possible AD from frontotemporal dementia.

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    • "Positron emission tomography is used to measure regional brain metabolism by 18F-deoxyglucose. A reduction in glucose metabolism in bilateral temporal parietal regions and the posterior cingulate has been proposed as diagnostic criteria for AD (Fig. 1D), with sensitivity and specificity of 88–95% and 62–74%, respectively [4]. Specific biomarkers of AD include amyloid-␤ 1-42 (A␤ 42 ), total tau (t-tau), and phospho-tau (p-tau). "
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    ABSTRACT: In Alzheimer's disease (AD) and dementia of the Alzheimer's type (DAT), the role played by peroxisomes is not well known. Peroxisomes are present in all eukaryotic cells, with the exception of erythrocytes. They are involved in the β-oxidation process of long-chain fatty acids, very-long-chain fatty acids, and branched-chain fatty acids. They participate in the α-oxidation of phytanic acid, the biosynthesis of bile acids, and the breakdown of eicosanoids. Peroxisomes are also involved in the synthesis of specific fatty acids such as docosahexaenoic acid (DHA), which is essential for the brain and retina, and plasmalogens (PLGN), which play crucial roles in neural cells and are essential components of myelin. Several studies conducted in animal models and in humans provided evidence for a role of DHA in preventing brain degeneration. Significantly lower levels of PLGN were observed in patients with severe dementia. Moreover, a decreased activity of carnitine acetyltransferase, an enzyme present in peroxisome (but also detected in mitochondria, endoplasmic reticulum, and nucleus), was reported in AD patients. We give an overview of the potential role of peroxisomes, especially in the part played by DHA, PLGN, carnitine, and carnitine-dependent peroxisomal enzymes, on the development of AD and DAT. The potential of developing novel therapies targeted on peroxisomal metabolism to prevent cognitive decline and other age-related neurological disorders is discussed.
    Journal of Alzheimer's disease: JAD 01/2012; 29(2):241-54. DOI:10.3233/JAD-2011-111163 · 4.15 Impact Factor
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    • "FDG PET studies in AD patients have demonstrated a typical pattern of reduced temporoparietal FDG uptake with sparing of the basal ganglia, thalamus and cerebellum (Coleman, 2005). Hypometabolism begins typically in the superior parietal cortex, then spreads inferiorly and anteriorly to involve the inferior parietal, superior temporal, and prefrontal cortices. "

    The Clinical Spectrum of Alzheimer's Disease -The Charge Toward Comprehensive Diagnostic and Therapeutic Strategies, 09/2011; , ISBN: 978-953-307-993-6
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    • "PET has been employed in many AD studies to examine the regional cerebral metabolic rate for glucose (rCMRGLc) using 18F-2-deoxy-2-fluoro-D-glucose as a marker. A reduction of glucose metabolism, as seen on PET in the bilateral temporal parietal regions and in the posterior cingulate, is the most commonly described diagnostic criterion for AD.53 A meta-analysis of nine studies revealed that the pooled sensitivity and specificity were both 86% for temporoparietal hypometabolism when discriminating AD patients from healthy controls.54 "
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    ABSTRACT: The pathophysiologic process of Alzheimer's disease (AD) begins years before the diagnosis of clinical dementia. This concept of preclinical AD has arisen from the observation of AD pathologic findings such as senile plaques and neurofibrillary tangles in the brains of people who at the time of death had normal cognitive function. Recent advances in biomarker studies now provide the ability to detect the pathologic changes of AD, which are antecedent to symptoms of the illness, in cognitively normal individuals. Functional and structural brain alterations that begin with amyloid-β accumulation already show the patterns of abnormality seen in individuals with dementia due to AD. The presence of preclinical AD provides a critical opportunity for potential interventions with disease-modifying therapy. This review focuses on the studies of antecedent biomarkers for preclinical AD.
    Journal of Clinical Neurology 06/2011; 7(2):60-8. DOI:10.3988/jcn.2011.7.2.60 · 1.70 Impact Factor
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