Ubisol-Q10 (a Nanomicellar Water-Soluble Formulation of CoQ10) Treatment Inhibits Alzheimer-Type Behavioral and Pathological Symptoms in a Double Transgenic Mouse (TgAPEswe, PSEN1dE9) Model of Alzheimer's Disease

Alzheimer's disease (AD) is one of the most common neurodegenerative pathologies for which there are no effective therapies to halt disease progression. Given the increase in the incidence of this disorder, there is an urgent need for pharmacological intervention. Unfortunately, recent clinical trials produced disappointing results. Molecular mechanisms of AD are converging on the notion that mitochondrial dysfunction, oxidative stress, and accumulation of dysfunctional proteins are involved in AD pathology. Previously, we have shown that a water-soluble formulation of Coenzyme Q(10) (Ubisol-Q(10)), an integral part of the electron transport chain, stabilizes mitochondria and prevents neuronal cell death caused by neurotoxins or oxidative stress both in vitro and in vivo. In this study, we evaluated the neuroprotective effects of Ubisol-Q(10) treatment in double transgenic AD mice. In the present study, we report that providing Ubisol-Q(10) in drinking water (at a dose of similar to 6 mg/kg/day) reduced circulating amyloid-beta (A beta) peptide, improved long term memory, preserved working spatial memory, and drastically inhibited A beta plaque formation in 18-month-old transgenic mice compared to an untreated transgenic group. Thus Ubisol-Q(10) supplementation has the potential to inhibit the progression of neurodegeneration, leading to a better quality of life for humans suffering with AD.