ParkinsonCanadaV1, Main, Exploration, bibRecord, 001620

Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia

Identifieur interne : 001620 ( Main/Exploration ); précédent : 001619; suivant : 001621

Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia

Auteurs : Tiffany W. Chow [Canada] ; Ariel Graff-Guerrero [Canada] ; Nicolaas Plg Verhoeff [Canada] ; Malcolm A. Binns [Canada] ; David F. Tang-Wai [Canada] ; Morris Freedman [Canada] ; Mario Masellis [Canada] ; Sandra E. Black [Canada] ; Alan A. Wilson [Canada] ; Sylvain Houle [Canada] ; Bruce G. Pollock [Canada]

Source :

Neuropsychiatric Disease and Treatment [ 1176-6328 ] ; 2011.

RBID : PMC:3140294

Abstract

Background

Memantine has shown effects on cortical metabolism in Alzheimer’s disease (AD), and the mechanism of action may not be specific to AD alone. We hypothesized that participants with frontotemporal dementia taking memantine would show an increased cortical metabolic activity in frontal regions, temporal regions, or in salience network hubs.

Methods

Sixteen participants with behavioral or language variant frontotemporal dementia syndromes (FTD) were recruited from tertiary FTD clinics and treated with memantine hydrochloride 10 mg twice daily in this fixed-dose, open-label pilot study. The primary endpoint was enhancement of cortical metabolic activity after 7–8 weeks of treatment. Secondary endpoints were measures of mood and behavior disturbance, frontal executive function, and motor disturbance.

Results

Voxel-wise parametric image analysis of positron emission tomography (PET) data from seven behavioral variant FTD patients, eight semantic dementia patients, and one progressive nonfluent aphasia patient, of mean age 64.3 years, mean duration of illness 4.25 years, and baseline mean sum of boxes Clinical Dementia Rating score 6.59, revealed an increase in [¹⁸F]-fluorodeoxyglucose (FDG) normalized metabolic activity in bilateral insulae and the left orbitofrontal cortex (P < 0.01). The increase on FDG-PET did not correlate with changes on behavioral inventories. Post hoc analysis indicated that semantic dementia participants drove this finding.

Conclusion

This open-label clinical PET study suggests that memantine induces an increase in metabolism in the salience network in FTD. A placebo-controlled follow-up study is warranted.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3140294

DOI: 10.2147/NDT.S22635
PubMed: 21792308
PubMed Central: 3140294

Affiliations:

Le document en format XML

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<author><name sortKey="Graff Guerrero, Ariel" sort="Graff Guerrero, Ariel" uniqKey="Graff Guerrero A" first="Ariel" last="Graff-Guerrero">Ariel Graff-Guerrero</name>
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<author><name sortKey="Tang Wai, David F" sort="Tang Wai, David F" uniqKey="Tang Wai D" first="David F" last="Tang-Wai">David F. Tang-Wai</name>
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</placeName>
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</affiliation>
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</affiliation>
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<author><name sortKey="Houle, Sylvain" sort="Houle, Sylvain" uniqKey="Houle S" first="Sylvain" last="Houle">Sylvain Houle</name>
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</placeName>
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</affiliation>
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<author><name sortKey="Pollock, Bruce G" sort="Pollock, Bruce G" uniqKey="Pollock B" first="Bruce G" last="Pollock">Bruce G. Pollock</name>
<affiliation wicri:level="4"><nlm:aff id="af4-ndt-7-415"> Department of Psychiatry, Division of Neurology, University of Toronto</nlm:aff>
<country>Canada</country>
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</placeName>
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<series><title level="j">Neuropsychiatric Disease and Treatment</title>
<idno type="ISSN">1176-6328</idno>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Memantine has shown effects on cortical metabolism in Alzheimer’s disease (AD), and the mechanism of action may not be specific to AD alone. We hypothesized that participants with frontotemporal dementia taking memantine would show an increased cortical metabolic activity in frontal regions, temporal regions, or in salience network hubs.</p>
</sec>
<sec><title>Methods</title>
<p>Sixteen participants with behavioral or language variant frontotemporal dementia syndromes (FTD) were recruited from tertiary FTD clinics and treated with memantine hydrochloride 10 mg twice daily in this fixed-dose, open-label pilot study. The primary endpoint was enhancement of cortical metabolic activity after 7–8 weeks of treatment. Secondary endpoints were measures of mood and behavior disturbance, frontal executive function, and motor disturbance.</p>
</sec>
<sec><title>Results</title>
<p>Voxel-wise parametric image analysis of positron emission tomography (PET) data from seven behavioral variant FTD patients, eight semantic dementia patients, and one progressive nonfluent aphasia patient, of mean age 64.3 years, mean duration of illness 4.25 years, and baseline mean sum of boxes Clinical Dementia Rating score 6.59, revealed an increase in [<sup>18</sup>
F]-fluorodeoxyglucose (FDG) normalized metabolic activity in bilateral insulae and the left orbitofrontal cortex (<italic>P</italic>
 < 0.01). The increase on FDG-PET did not correlate with changes on behavioral inventories. Post hoc analysis indicated that semantic dementia participants drove this finding.</p>
</sec>
<sec><title>Conclusion</title>
<p>This open-label clinical PET study suggests that memantine induces an increase in metabolism in the salience network in FTD. A placebo-controlled follow-up study is warranted.</p>
</sec>
</div>
</front>
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</affiliations>
</record>

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La maladie de Parkinson au Canada (serveur d'exploration)

Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia

Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia

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	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.