Positron Emission Tomography Imaging in Dementia

Positron Emission Tomography Imaging in Dementia

Herholz Karl
Published: European Neurology - Volume 3 Issue 2
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Positron emission tomography (PET) utilises biologically active molecules in micromolar or nanomolar concentrations that have been labelled with shortlived positron-emitting isotopes. The physical characteristics of the isotopes and the molecular specificity of labelled molecules, combined with the high detection efficacy of modern PET scanners, provide sensitivity for in vivo measurement that is several orders of magnitude higher than with the other imaging techniques. While the very short half-lives of 15O (two minutes) and 11C (20 minutes) limit their use to fully equipped PET centres with a cyclotron and radiopharmaceutical laboratory, 18F-labelled tracers (half-life 110 minutes) can be produced in specialised cyclotron centres for regional distribution to hospitals running a PET scanner only.

Glucose is the main energy supply for the brain. Its metabolism maintains ion gradients and glutamate turnover and is closely coupled to neuronal function at rest and during functional activation.1 Its measurement by 18F-2- fluoro-2-deoxy-D-glucose (FDG) is based on phosphorylation of the tracer by hexokinase, which is the pivotal first step of that metabolic pathway. Typically, PET images are obtained 30–60 minutes after tracer injection, when FDG uptake is approximately proportional to glucose metabolism, and actual measurement times can be as short as five to 10 minutes. Under resting conditions (awake, but without external stimulation), normal grey matter displays two to four times higher glucose metabolism than white matter. There is a moderate reduction of cerebral glucose metabolism with age, mainly affecting the frontal association cortex.2 Significant regional reductions of glucose metabolism indicate impairment of synaptic function, and the technique is therefore applicable to all types of dementia.

There is growing interest in imaging amyloid deposits, the pathological hallmarks of Alzheimer’s disease (AD). There are now several PET tracers for in vivo amyloid imaging that allow longitudinal studies of amyloid deposition to clarify whether amyloid deposition is a cause or consequence in the pathophysiology of AD.3,4 Furthermore, the degeneration of major neurotransmitter systems can be demonstrated in vivo by using appropriate PET tracers. Impairment of the cholinergic and dopaminergic neurotransmission is of particular diagnostic interest. By these means, PET can detect early stages and differentiate between various types of dementia, and also monitor progression and the effect of therapeutic intervention.

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