Studies of Cerebral Metabolism and Blood Flow in Dementia

Studies with FDG PET in Alzheimer's patients revealed a typical hypometabolism in neocortical structures, mainly the parietal, frontal, and posterior temporal association cortices, that is the same areas where neuronal as well as synaptic degenerations are most severe in postmortem studies. In addition to the regional abnormalities, these patients also exhibit a global reduction of cerebral glucose metabolism. Metabolic decrease in the parieto-temporal association cortex has been recognized as potentially diagnostic for Alzheimer's disease, and this recognition has facilitated the use of PET in clinical settings to evaluate patients with dementia. Also suggestive of dementia of Alzheimer's type (DAT) are: bilateral metabolic reduction in the parieto-temporal association cortex; glucose metabolism reduction in the frontal association cortex, mainly in advanced disease; relative preservation of primary neocortical structures, such as the sensorimotor and primary visual cortex, and also of subcortical structures, like basal ganglia, brainstem, and thalamus; and variable presentation of metabolic reduction in the mesial temporal cortex. A high diagnostic accuracy by FDG PET in the initial assessment of suspected DAT patients, and those who will subsequently be diagnosed with DAT, can be achieved by using such criteria as prefrontal and/or bilateral temporo-parietal hypometabolism. Longitudinal PET studies in DAT patients showed an expansion as well as an increased severity of hypometabolism in associated cortical areas and subcortical structures, and a close correlation between progressive metabolic reduction and impaired cognitive performance has been shown.

Recently, ligands were developed that bind to amyloid plaques, which are specific for DAT. 1-(1-{6-[(2-[18F]fluoroethyl)(methyl)amino]-2-[naphthyl}ethylidene)malo-nonitrile ([18F]FDDNP) in conjunction with PET allows for the determination of localization and load of neurofibrillary tangles (NFTs) and beta-amyloid senile plaques

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