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Updated: May 30, 2026
Radiotracer Administration for High Temporal Resolution Positron Emission Tomography of the Human Brain: Application to FDG-fPET
Published on: October 22, 2019
Open-label study of the short-term effects of memantine on FDG-PET in frontotemporal dementia
Tiffany W Chow1, Ariel Graff-Guerrero, Nicolaas Plg Verhoeff
1Division of Neurology, Baycrest.
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 [(18)F]-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.
Insights
Memantine increased brain metabolism in frontotemporal dementia (FTD) patients, particularly in the salience network. This suggests memantine may benefit FTD by enhancing cortical activity, warranting further placebo-controlled studies.
Area of Science:
- Neuroscience
- Neurology
- Pharmacology
Background:
- Memantine's effects on cortical metabolism in Alzheimer's disease (AD) suggest its mechanism may extend beyond AD.
- This study investigated memantine's impact on cortical metabolic activity in frontotemporal dementia (FTD).
Purpose of the Study:
- To test the hypothesis that memantine increases cortical metabolic activity in frontal and temporal regions or salience network hubs in FTD patients.
- To evaluate memantine's effects on mood, behavior, executive function, and motor disturbances in FTD.
Main Methods:
- An open-label pilot study involving 16 participants with behavioral or language variant FTD syndromes.
- Participants received memantine hydrochloride 10 mg twice daily for 7-8 weeks.
- Primary endpoint: enhanced cortical metabolic activity via [18F]-fluorodeoxyglucose (FDG)-PET scans.
Main Results:
- FDG-PET revealed increased normalized metabolic activity in bilateral insulae and the left orbitofrontal cortex (P < 0.01).
- The observed metabolic increase did not correlate with behavioral changes.
- Post hoc analysis indicated semantic dementia patients primarily drove the metabolic findings.
Conclusions:
- Memantine appears to induce increased metabolism within the salience network in FTD patients.
- These findings suggest memantine's potential therapeutic role in FTD.
- A placebo-controlled follow-up study is recommended to confirm these results.
