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PET Project

Positron emission tomography (PET) uses biologically active molecules in micromolar or nanomolar concentrations that have been labelled with short-lived positron emitting isotopes. PET can detect pathological alterations of brain tissue function and their changes during treatment in living subjects with Alzheimer’s disease (AD) with a sensitivity and specificity that is higher than with other imaging techniques. Currently, two approaches are being used in clinical drug trials: measurement of cerebral glucose metabolism by 18F-2-fluoro-2-deoxy- D-glucose (FDG) to assess impairment of synaptic function, and specific tracers for pathological amyloid which have been developed recently.

FDG PET

Brain glucose metabolism is assessed by PET images which are obtained typically 30 to 60 minutes after intravenous injection of 200 to 400 MBq of FDG, with scanning times that can be as short as five minutes. FDG uptake at that time is approximately proportional to cerebral glucose metabolism, which in turn is largely dependent on synaptic function. Studies are usually performed in a resting state without specific cognitive stimulation and, in contrast to some applications of PET in neuroscience research, there is no need to take blood samples. Under these easily tolerated conditions, FDG uptake in most grey matter areas is two to three times as high as in white matter in normal subjects. There are regional differences, with the highest values in striatum and parietal cortex close to the parieto-occipital sulcus. Some phylogenetically older brain structures such as the medial temporal cortex and cerebellum have metabolic rates below the grey matter average, but are still higher than normal white matter. There is a moderate reduction of cerebral glucose metabolism with age in normal subjects, mainly affecting frontal association cortex.

In AD, FDG uptake is reduced significantly by up to 50 per cent, mainly in temporal-parietal association cortices including the posterior cingulate cortex. Frontal association cortex may also be involved, but more variably so and mostly after progression to severe dementia. In contrast to other diseases that may lead to dementia such as ischemic stroke, glucose metabolism in basal ganglia, primary motor and visual cortex, and cerebellum is usually well preserved in AD. This pattern generally reflects AD clinical symptoms with impaired memory and associative thinking, while primary motor and sensory function are relatively preserved until the very late stages of the disease. It is typically most clearly seen in AD patients with disease onset before the age of 65 (early onset AD), while late onset AD patients may also have some impairment of basal ganglia and motor areas, most likely due to chronic cerebrovascular disease and generalised age-associated brain atrophy. In studies with pathological confirmation of diagnosis, sensitivity ranged from 84 to 98 per cent and specificity from 71 to 74 per cent (1,2).


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Karl Herholz graduated as a medical doctor from the University of Erlangen, Germany, in 1980. After basic general clinical training, he joined the Max-Planck-Institute for Neurological Research in Cologne, Germany, as a research fellow in 1982, and became Professor of Neurology at the University of Cologne in 1994. He moved to the University of Manchester, UK, in 2005 to become Professor in Clinical Neuroscience and Director of the Wolfson Molecular Imaging Centre. His research focuses on neuroimaging studies (PET and MRI) of dementia and brain tumours. He has published more than 250 research papers, and received prizes from the Max-Planck- Society and the Hirnliga.
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Karl Herholz
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