Journal
DEMENTIA AND GERIATRIC COGNITIVE DISORDERS EXTRA
Volume 7, Issue 2, Pages 204-214Publisher
KARGER
DOI: 10.1159/000477343
Keywords
Alzheimer disease; FDG-PET; Rifampicin; Amyloid-beta; Oligomer; Preventive therapy
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Background: Rifampicin was reported to inhibit amyloid-beta oligomerization and tau hyperphosphorylation in mouse models and could serve as a promising available medicine for the prevention of Alzheimer disease (AD). To examine whether rifampicin has such preventive effects in humans, we retrospectively reviewed F-18-FDG-PET findings of elderly patients with mycobacterium infection treated with rifampicin. Methods: Forty nondemented elderly patients treated with rifampicin for mycobacterium infections who showed AD-type hypometabolism were enrolled. The hypometabolic patterns were evaluated with stereotaxic statistical analysis and region of interest analysis. Results: Before treatment, AD-type hypometa-bolism was observed in 12 patients. The FDG uptake in the posterior cingulate cortex (PCC) was improved or stabilized in 6 patients after 12-month therapy (450 mg/day), whereas another 6 patients with 6-month therapy showed a decreased FDG uptake in the PCC. In patients who underwent FDG-PET only after treatment, the metabolic decline in the PCC was significantly milder in patients with >= 12 months of rifampicin treatment than in those with 6 months of treatment. Multiple regression analysis revealed that the dose of rifampicin and treatment duration significantly influenced FDG uptake in the PCC. Conclusion: The preventive effect of rifampicin depended on the dose and the treatment duration, and the effect needs at least 450 mg daily for 1 year. c 2017 The Author(s) Published by S. Karger AG, Basel
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