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Diet supplement CoQ 10 delays brain atrophy in aged transgenic mice with mutations in the amyloid precursor protein: An in vivo volume MRI study
Author(s) -
Li Geng,
Jack Clifford R.,
Yang XiFei,
Yang Edward S.
Publication year - 2008
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520320120
Subject(s) - presenilin , genetically modified mouse , atrophy , amyloid precursor protein , in vivo , hippocampus , transgene , medicine , endocrinology , wild type , hippocampal formation , chemistry , pathology , psychology , biology , alzheimer's disease , biochemistry , mutant , genetics , disease , gene
We tested the hypotheses that supplemental intake of the diet supplement Coenzyme Q 10 (CoQ 10 ) could delay brain atrophy in double transgenic amyloid precursor protein (APP) / presenilin 1 (PS1), single transgenic APP and PS1 as well as wild type mice by volume MR image in vivo . One hundred and twelve mice (28 APP/PS1, 28 APP, 28 PS1 and 28 wild types) were studied. Half of each genotype group ( n = 14 per group) was treated with CoQ 10 2400 mg/kg/day, and the other half with placebo for 60 days. Magnetic resonance (MR) images were used to obtain the volumes of the hemispheres and hippocampi. APP / PS1, APP, PS1 and wild type mice treated with CoQ 10 exhibited significantly less atrophy in hemisphere and hippocampus than those receiving placebo. The neuro‐protective effect of the CoQ 10 on hemispheric volume, and hippocampal volume was related to genotype; greater in APP/PS1 than APP and PS1 mice and less in wild type mice. Our result indicated that CoQ 10 may have therapeutic potential in the prevention and treatment of MCI and AD.