[18F]FDG PET is a well-established method for the evaluation of patients with suspected Alzheimer's disease (AD) and other neurodegenerative diseases [1]. This tool has the unique ability to estimate the local cerebral metabolic rate of glucose consumption (CMRgl), thus providing information on the distribution of neuronal death and synapse dysfunction in vivo [2]. Clinically, [18F]FDG PET plays a major role in the early and differential diagnosis of dementia due to AD by showing specific disease patterns of hypometabolism, reflecting neuronal dysfunction in affected brain regions even in the earliest stages of the disease [1]. However, the role of [18F]FDG PET in identifying patients affected by AD but who are still at the stage of mild cognitive impairment (MCI) is less established. Although various studies have indicated a high predictive value in this population, appropriate standardization approaches (i.e. semiquantification methods, observer-independent analyses, identification of cut-off values) and the value of [18F]FDG PET in comparison to amyloidosis biomarkers are still a matter of debate. Recently, a Cochrane review was published with the objective of determining the diagnostic accuracy of [18F]FDG PET for identifying subjects with MCI who will clinically convert toADor other dementias [3]. The authors concluded that there is no evidence supporting routine clinical use of [18F]FDG PET to identify those patients with MCI who will develop AD. For several reasons, we do not agree with the authors of this Cochrane review that existing data on the value of FDG PET in MCI supports such a categorical conclusion. Indeed, clear variability in diagnostic performance of [18F]FDG PET is found in the literature, as correctly reported in the Cochrane review. This variability, however, is not exclusively attributable to the method itself, but rather can be explained by a number of factors concerning study design, definitions of MCI itself and data analysis procedures. We would like to highlight some of these factors in greater detail, because we believe that knowledge on these issues may be necessary to correctly interpret the available literature and to appreciate the diagnostic value of [18F]FDG PET in MCI.
A Cochrane review on brain 18F-FDG PET in dementia: limitations and future perspectives
Pappata' S;Pagani M
2015
Abstract
[18F]FDG PET is a well-established method for the evaluation of patients with suspected Alzheimer's disease (AD) and other neurodegenerative diseases [1]. This tool has the unique ability to estimate the local cerebral metabolic rate of glucose consumption (CMRgl), thus providing information on the distribution of neuronal death and synapse dysfunction in vivo [2]. Clinically, [18F]FDG PET plays a major role in the early and differential diagnosis of dementia due to AD by showing specific disease patterns of hypometabolism, reflecting neuronal dysfunction in affected brain regions even in the earliest stages of the disease [1]. However, the role of [18F]FDG PET in identifying patients affected by AD but who are still at the stage of mild cognitive impairment (MCI) is less established. Although various studies have indicated a high predictive value in this population, appropriate standardization approaches (i.e. semiquantification methods, observer-independent analyses, identification of cut-off values) and the value of [18F]FDG PET in comparison to amyloidosis biomarkers are still a matter of debate. Recently, a Cochrane review was published with the objective of determining the diagnostic accuracy of [18F]FDG PET for identifying subjects with MCI who will clinically convert toADor other dementias [3]. The authors concluded that there is no evidence supporting routine clinical use of [18F]FDG PET to identify those patients with MCI who will develop AD. For several reasons, we do not agree with the authors of this Cochrane review that existing data on the value of FDG PET in MCI supports such a categorical conclusion. Indeed, clear variability in diagnostic performance of [18F]FDG PET is found in the literature, as correctly reported in the Cochrane review. This variability, however, is not exclusively attributable to the method itself, but rather can be explained by a number of factors concerning study design, definitions of MCI itself and data analysis procedures. We would like to highlight some of these factors in greater detail, because we believe that knowledge on these issues may be necessary to correctly interpret the available literature and to appreciate the diagnostic value of [18F]FDG PET in MCI.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
