Coenzyme Q10 attenuates β-amyloid pathology in the aged transgenic mice with Alzheimer presenilin 1 mutation

One of the neuropathological features of Alzheimer’s disease (AD) is the deposition of senile plaques containing β-amyloid (Aβ). There is limited evidence for the treatment to arrest Aβ pathology of AD. In the present study, they tested the effect of coenzyme Q10 (CoQ10), an endogenous antioxidant and a powerful free radical scavenger, on Aβ in the aged transgenic mice overexpressing Alzheimer presenilin 1-L235P (leucine-to-proline mutation at codon 235, 16–17 months old). The treatment by feeding the transgenic mice with CoQ10 for 60 days (1,200 mg kg−1 day−1) partially attenuated Aβ overproduction and intracellular Aβ deposit in the cortex of the transgenic mice compared with the age-matched untreated transgenic mice. Meanwhile, an increased oxidative stress reaction was detected as evidenced by elevated level of malondialdehyde (MDA) and decreased activity of superoxide dismutase (SOD) in the transgenic mice relative to the wild-type mice, and supplementation of CoQ10 partially decreased MDA level and upregulated the activity of SOD. The results indicate that oxidative stress is enhanced in the brain of the transgenic mice, that this enhancement may further promote Aβ42 overproduction in a vicious formation, and that CoQ10 would be beneficial for the therapy of AD.