Effect of Piracetam on Cerebral Glucose Metabolism in Alzheimer's Disease as Measured by Positron Emission Tomography

Abstract

Summary:The effect of piracetam (a putative enhancer of cerebral metabolism) on regional CMRalu was studied by positron emission tomography of 2[18Fl-fluoro-2-deoxY-D-glucose in nine patients with Alzheimer's dis ease, and in seven cases with multiinfarct dementia or unclassified dementia. In Alzheimer's disease, i. v. ad ministration of piracetam, 6 g b.i.d. for 2 weeks, signifi cantly improved rCMRalu in most cortical areas, whereas no effect on CMRalu of the drug was observed in the mul tiinfarct dementia/unclassified dementia groups. These

Evaluation of a Calibrated 18F-FDG PET Score as a Biomarker for Progression in Alzheimer Disease and Mild Cognitive Impairment

“…In most of these trials the emphasis was on examining whether the drug would increase cerebral glucose metabolism as a pharmacodynamic effect of treatment rather than on assessment of progression. Typically these were short trials of a few weeks or up to 3 mo active treatment duration with 18 F-FDG PET before and during treatment (20)(21)(22). Trials that were extended for at least 6 mo also showed evidence of disease progression by further reduction of glucose metabolism in association cortices (23)(24)(25)(26).…”

Decreased glucose utilization in the striatum and frontal lobe in probable striatonigral degeneration

“…The diagnosis of SND is based on clinical signs and evolution, particularly an absent or evanescent response to L-dopa 19, lo}. Computed tomography (CT) and magnetic resonance imaging (MRI) may reveal atrophy and iron deposits in the striaturn 111-131, but the specificity of these findings gional cerebral glucose metabolism and brain morphological features were studied in 7 patients with probable SND using positron emission tomography (PET) with "F-labeled 2-deoxy-2-fluoro-D-glucose (FDG) as the tracer and proton MRI.…”

Effect of Phosphatidylserine on Cerebral Glucose Metabolism in Alzheimer's Disease

“…In these impaired synapses with limited function, PS might be most effective. The nonselective increase in rCMRGl similar to that described for the metabolic enhancer pira cetam [26] is distinctly different from the selective ac tion of a muscarinergic cholinagonist which, during a 6-week treatment period, prevented the deterioration of glucose metabolism in areas typically involved in AD, while CMRG1 in other areas further decreased during treatment [27], Despite the preliminary character of this study, our data showed a significant effect of PS on regional glucose metabolism in a small number of AD patients. These data may form the basis for a larger clinical trial with a longer duration of PS treatment in which various mea sures of cognitive performance, neuropsychological defi cits.…”