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

J Alzheimers Dis. 2018;61(1):221-236. doi: 10.3233/JAD-170275.


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 Q10 (Ubisol-Q10), 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-Q10 treatment in double transgenic AD mice. In the present study, we report that providing Ubisol-Q10 in drinking water (at a dose of ∼6 mg/kg/day) reduced circulating amyloid-β (Aβ) peptide, improved long term memory, preserved working spatial memory, and drastically inhibited Aβ plaque formation in 18-month-old transgenic mice compared to an untreated transgenic group. Thus Ubisol-Q10 supplementation has the potential to inhibit the progression of neurodegeneration, leading to a better quality of life for humans suffering with AD.

Keywords: Alzheimer’s disease; CoQ10; amyloid-β plaques; long term memory; working memory.

MeSH terms

  • Alzheimer Disease / complications*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / blood*
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Disease Models, Animal
  • Male
  • Maze Learning / drug effects
  • Memory / drug effects
  • Memory Disorders / drug therapy*
  • Memory Disorders / etiology*
  • Mice
  • Mice, Transgenic
  • Microglia / drug effects
  • Microglia / pathology
  • Mutation / genetics
  • Nerve Tissue Proteins / metabolism
  • Peptide Fragments / blood*
  • Presenilin-1 / genetics
  • Ubiquinone / analogs & derivatives*
  • Ubiquinone / therapeutic use
  • Vitamins / therapeutic use*


  • APP protein, human
  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Nerve Tissue Proteins
  • PSEN1 protein, human
  • Peptide Fragments
  • Presenilin-1
  • Vitamins
  • amyloid beta-protein (1-40)
  • Ubiquinone
  • coenzyme Q10