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P2‐075: FDG‐PET studies in early‐onset familial Alzheimer's disease
Author(s) -
Schöll Michael,
Stefanova Elka,
Almkvist Ove,
Axelman Karin,
Wall Anders,
Långström Bengt,
Lannfelt Lars,
Viitanen Matti,
Nordberg Agneta
Publication year - 2008
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2008.05.1148
Subject(s) - medicine , mutation , neuropsychology , statistical parametric mapping , dementia , gene mutation , oncology , disease , pathology , psychology , genetics , gene , psychiatry , cognition , biology , magnetic resonance imaging , radiology
sults: Overall, 32/37 randomized patients completed 26 weeks, and 24/37 patients completed 52 weeks. At week 52, the reduction in total brain volume was similar between memantine and placebo groups, but the reduction in hippocampal volume was markedly less for memantine-treated patients (2.4%), as compared with placebo-treated patients (4.0%). Memantine-treated patients also showed less annual decline in glucose metabolism in all brain areas, as compared with placebo. There was no clear trend in NAA and MI concentrations over time in either patient group, but intra-individual variability was large. In clinical measures, memantine-treated patients showed a slower rate of decline than placebo-treated patients. No study outcomes reached statistical significance versus placebo, due to the small sample size of this pilot study. Conclusions: This study indicates that memantine slows the progression of hippocampal atrophy in patients with mild to moderate AD, which is in line with its suggested neuroprotective effect. These results also suggest that memantine slows the decline in glucose metabolism, indicating beneficial functional effects. Clinical outcomes of this study were consistent with previous observations, with memantine demonstrating a favorable effect versus placebo.