title: Positron emission tomography imaging in dementia.
abstract: Positron emission tomography (PET) is a well-established imaging modality. Measurement of regional cerebral glucose metabolism (rCMR(glc)) using PET and [(18)F]-2-fluoro-2-deoxy-D-glucose (FDG) has become a standard technique in both oncology and dementia research. When measuring rCMR(glc) in Alzheimer's disease (AD), characteristic reductions in rCMR(glc) are found in neocortical association areas including the posterior cingulate, precuneus, temporoparietal and frontal multimodal association regions; the primary visual cortex, sensorimotor cortex, basal ganglia and cerebellum are relatively unaffected. FDG-PET has been used in the study of mild cognitive impairment (MCI) to accurately predict the subsequent decline to AD. Impairment in rCMR(glc) may be seen in individuals at high genetic risk of AD, even before clinical symptoms are apparent. Characteristic patterns of regional hypometabolism are also seen in other degenerative dementias such as frontotemporal dementia (FTD) and dementia with Lewy bodies (DLB). The use of different radioisotopes and tracers increases the versatility of PET. Tracers adopted in dementia research include (11)C-PK-11195 and (11)C-PIB, which have been used to investigate neuroinflammation and amyloid deposition, respectively, in both AD and MCI populations. It is also possible to investigate neurotransmitter systems in dementia; targets have included the cholinergic, dopaminergic and serotonergic systems. Imaging the brains of dementia patients using PET provides important information about the brain function of these individuals that would otherwise be unavailable with other imaging modalities. PET will continue to be important in future dementia research as new tracers become available to help in the early and specific diagnosis of increasingly well-defined clinical syndromes, and assist in the assessment of new therapeutic interventions.
authors.affiliation: Wolfson Molecular Imaging Centre, University of Manchester, Manchester, UK. Karl.Herholz@manchester.ac.uk
authors.forename: K
authors.initials: K
authors.lastname: Herholz
authors.forename: S F
authors.initials: SF
authors.lastname: Carter
authors.forename: M
authors.initials: M
authors.lastname: Jones
mesh_terms: D000544:Alzheimer Disease / Q000000981:diagnostic imaging; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism; D003072:Cognition Disorders / Q000209:etiology; D003704:Dementia / Q000000981:diagnostic imaging* / Q000378:metabolism; D019788:Fluorodeoxyglucose F18; D006801:Humans; D020961:Lewy Body Disease / Q000000981:diagnostic imaging; D018377:Neurotransmitter Agents / Q000378:metabolism; D049268:Positron-Emission Tomography / Q000379:methods*; D019275:Radiopharmaceuticals
chemical_list: D001786:Blood Glucose; D018377:Neurotransmitter Agents; D019275:Radiopharmaceuticals; D019788:Fluorodeoxyglucose F18