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Emission tomography in dementia

Lookup NU author(s): Dr Sanjeet Pakrasi, Professor John O'Brien

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Abstract

Dementia is a chronic brain syndrome with enormous impact on health care provision. Emission tomography (single photon emission computed tomography (SPECT) and positron emission tomography (PET)) provides a unique tool to investigate functional and neurochemical changes, both in those with established dementia and in those at risk of subsequent cognitive decline. Alzheimer ' s disease is characterized by bilateral temporoparietal hypoperfusion on SPECT and hypometabolism on PET, which may precede the onset of dementia as similar changes can be demonstrated in those with mild cognitive impairment and in those genetically at risk of developing Alzheimer's disease. In dementia with Lewy bodies medial parietal and occipital perfusion deficits are seen together with pre-synaptic and post-synaptic dopaminergic changes, most particularly a reduction in the striatal presynaptic dopamine transporter which can be visualized using appropriate ligands (e.g., I-123-FP-CIT). Vascular dementia is associated with multiple, asymmetric, perfusion deficits in multi-infarct dementia. In contrast, subcortical vascular dementia is associated with reduced perfusion but preserved oxygen extraction fraction on PET Fronto-temporal dementia is characterized by both hypometabolism and hypoperfusion in fronto-temporal lobes, though hypornetabolism appears more extensive, affecting large areas of the cerebral hemispheres. Longitudinal studies of treatment response in Alzheimer's disease with cholinergic drugs have found changes in regional blood flow and nicotinic and muscarinic receptor function in those patients who respond to treatment. Currently, emission tomography is widely used for assisting with clinical differential diagnosis. Future developments will entail the development and application of more specific neurochernical ligands and those which bear a closer relationship to the underlying disease processes, including markers of tau, amyloid and synuclein pathology. Nucl Med Commun 26:189-196 (c) 2005 Lippincott Williams D Wilkins.


Publication metadata

Author(s): Pakrasi S, O'Brien JT

Publication type: Review

Publication status: Published

Journal: Nuclear Medicine Communications

Year: 2005

Volume: 26

Issue: 3

Pages: 189-196

ISSN (print): 0143-3636

ISSN (electronic): 1473-5628

URL: http://dx.doi.org/10.1097/00006231-200503000-00003

DOI: 10.1097/00006231-200503000-00003


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