Can FDG-PET predict who is to rapidly convert to Alzheimer's disease?
University of Cambridge, Cambridge, England, United Kingdom Neurology
(Impact Factor: 8.29).
05/2003; 60(8):1374-7. DOI: 10.1212/01.WNL.0000055847.17752.E6
Patients with mild cognitive impairment (MCI) were assessed, and a metabolic profile associated with conversion to AD at 18-month follow-up was sought. As compared with nonconverters (n = 10), converters (n = 7) had lower fluorodeoxyglucose uptake in the right temporoparietal cortex (p = 0.02, corrected for cluster size), without individual overlap. Awaiting replication in an independent sample, these findings suggest that among patients with MCI, fluorodeoxyglucose PET may accurately identify rapid converters.
Available from: Shailendra Segobin
- "The functional activity of the brain is known to be altered in diseases, even when at rest. It has therefore been subject to several studies through which the functional alterations of memory systems were observed notably in patients with Mild Cognitive Impairment (Chételat et al. 2003b) and AD (Desgranges et al. 1998, 2002; Eustache et al. 2004; Rauchs et al. 2007). In fact, the success of PET in studying brain networks at rest has led to the application of that principle to the now ever-growing concept of resting state functional MRI (RS-fMRI). "
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ABSTRACT: Measurement of synaptic activity by Positron Emission Tomography (PET) and its relation to cognitive functions such as episodic memory, working memory and executive functions in healthy humans and patients with neurocognitive disorders have been well documented. In this review, we introduce the concept of PET imaging that allows the observation of a particular biological process in vivo through the use of radio-labelled compounds, its general use to the medical world and its contributions to the understanding of memory systems. We then focus on [(18)F]-2-fluoro-2-deoxy-D-glucose (FDG-PET), the radiotracer that is used to measure local cerebral metabolic rate of glucose that is indicative of synaptic activity in the brain. FDG-PET at rest has been at the forefront of functional neuroimaging over the past 3 decades, contributing to the understanding of cognitive functions in healthy humans and how these functional patterns change with cognitive alterations. We discuss methodological considerations that are important for optimizing FDG-PET imaging data prior to analysis. We then highlight the contribution of FDG-PET to the understanding of the patterns of functional differences in non-degenerative pathologies, normal ageing, and age-related neurodegenerative disorders. Through reasonable temporal and spatial resolution, its ability to measure synaptic activity in the whole brain, independently of any specific network and disease, makes it ideal to observe regional functional changes associated with memory impairment.
Available from: Chiara Cerami
- "To increase diagnostic reliability in early phases of the disease process and make statistically informed decisions about metabolic abnormalities associated with dementia, it is important to increase normalization accuracy in order to reduce random effects due to noise present in individual images, which is especially prevalent in PET (Markiewicz et al. 2009). Our group analyses revealed higher statistical sensitivity with normalization to the [ 18 F]-FDG PET dementia-specific template, in relation to the existing [ 15 O]- H2O normalization procedure (see Figure 5) in areas with typically decreased glucose metabolism in AD (Herholz et al. 2002; Teune et al. 2010; Chételat et al. 2003), bvFTD (Teune et al. 2010; Salmon et al. 2003) and DLB (Teune et al. 2010; Minoshima et al. 2001). With respect to the DLB group, occipital hypometabolism has been shown to be a specific topographical marker of this dementia subtype (Minoshima et al. 2001); associated with DLB-specific clinical symptoms, such as visual hallucinations (Mori et al. 2006) that play a key role in the differential diagnosis with respect to AD (McKeith et al. 2005). "
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ABSTRACT: [18F]-fluorodeoxyglucose (FDG) Positron Emission Tomography (PET) is a widely used diagnostic tool that can detect and quantify pathophysiology, as assessed through changes in cerebral glucose metabolism. [18F]-FDG PET scans can be analyzed using voxel-based statistical methods such as Statistical Parametric Mapping (SPM) that provide statistical maps of brain abnormalities in single patients. In order to perform SPM, a "spatial normalization" of an individual's PET scan is required to match a reference PET template. The PET template currently used for SPM normalization is based on [15O]-H2O images and does not resemble either the specific metabolic features of [18F]-FDG brain scans or the specific morphological characteristics of individual brains affected by neurodegeneration. Thus, our aim was to create a new [18F]-FDG PET aging and dementia-specific template for spatial normalization, based on images derived from both age-matched controls and patients. We hypothesized that this template would increase spatial normalization accuracy and thereby preserve crucial information for research and diagnostic purposes. We investigated the statistical sensitivity and registration accuracy of normalization procedures based on the standard and new template-at the single-subject and group level-independently for subjects with Mild Cognitive Impairment (MCI), probable Alzheimer's Disease (AD), Frontotemporal lobar degeneration (FTLD) and dementia with Lewy bodies (DLB). We found a significant statistical effect of the population-specific FDG template-based normalisation in key anatomical regions for each dementia subtype, suggesting that spatial normalization with the new template provides more accurate estimates of metabolic abnormalities for single-subject and group analysis, and therefore, a more effective diagnostic measure
Available from: Niklas Mattsson
- "Alzheimer's disease is the most common cause of dementia, and is associated with accumulation of amyloid-b, tau, and progressive brain atrophy (Blennow et al., 2006). Early in the development of Alzheimer's disease, brain function in specific regions is reduced, as reflected by regionally reduced glucose metabolism (Friedland et al., 1983, 1989; Reiman et al., 1996; Silverman et al., 2001; Ché telat et al., 2003; Mosconi et al., 2005, 2008) and cerebral blood flow (CBF) (Johnson et al., 1987; Ishii et al., 1997) measured by PET. Moreover, brain accumulation of amyloid-b is associated with both brain atrophy and CBF changes, as detected by 15 O-H 2 O PET in cognitively healthy controls (Sojkova et al., 2008). "
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ABSTRACT: Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. Using 182 subjects from the Alzheimer's Disease Neuroimaging Initiative we tested associations of amyloid-β with regional cerebral blood flow in healthy controls (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with dementia (n = 24). Based on the theory that Alzheimer's disease starts with amyloid-β accumulation and progresses with symptoms and secondary pathologies in different trajectories, we tested if cerebral blood flow differed between amyloid-β-negative controls and -positive subjects in different diagnostic groups, and if amyloid-β had different associations with cerebral blood flow and grey matter volume. Global amyloid-β load was measured by florbetapir positron emission tomography, and regional blood flow and volume were measured in eight a priori defined regions of interest. Cerebral blood flow was reduced in patients with dementia in most brain regions. Higher amyloid-β load was related to lower cerebral blood flow in several regions, independent of diagnostic group. When comparing amyloid-β-positive subjects with -negative controls, we found reductions of cerebral blood flow in several diagnostic groups, including in precuneus, entorhinal cortex and hippocampus (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior temporal cortex (early and late mild cognitive impairment and dementia). The associations of amyloid-β with cerebral blood flow and volume differed across the disease spectrum, with high amyloid-β being associated with greater cerebral blood flow reduction in controls and greater volume reduction in late mild cognitive impairment and dementia. In addition to disease stage, amyloid-β pathology affects cerebral blood flow across the span from controls to dementia patients. Amyloid-β pathology has different associations with cerebral blood flow and volume, and may cause more loss of blood flow in early stages, whereas volume loss dominates in late disease stages.
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