tocopherylquinone has been researched along with Alzheimer-Disease* in 2 studies
1 trial(s) available for tocopherylquinone and Alzheimer-Disease
Article | Year |
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Concentrations of alpha-tocopherol and its quinone derivative in cerebrospinal fluid from patients with vascular dementia of the Binswanger type and Alzheimer type dementia.
We determined the concentrations of alpha-tocopherol (alpha-TOH) and alpha-tocopherol quinone(alpha-TQ), an oxidized derivative of alpha-TOH, in cerebrospinal fluid from patients with Alzheimer type dementia (ATD) and those with vascular dementia of the Binswanger type (VDBT). Compared with results for the controls, the VDBT patients had unaltered concentrations of alpha-TOH, but a statistically significant, 3.6-fold increase of alpha-TQ (P < 0.01) which was significantly correlated with decreases in the Mini-Mental State Examination scores (P < 0.05). In contrast, ATD patients had significantly decreased concentrations of alpha-TOH (P < 0.01), but had unaltered concentrations of alpha-TQ. These results suggest that there is greater oxidation of alpha-TOH to alpha-TQ in VDBT brain, but are inconclusive about the occurrence of peroxidation in ATD brains. Topics: Aged; Aging; Alzheimer Disease; Arteriosclerosis; Dementia, Vascular; Humans; Lipid Peroxides; Psychiatric Status Rating Scales; Vitamin E | 1994 |
1 other study(ies) available for tocopherylquinone and Alzheimer-Disease
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Alpha-tocopherol quinine ameliorates spatial memory deficits by reducing beta-amyloid oligomers, neuroinflammation and oxidative stress in transgenic mice with Alzheimer's disease.
The pathologies of Alzheimer's disease (AD) is associated with soluble beta-amyloid (Aβ) oligomers, neuroinflammation and oxidative stress. Decreasing the levels of Aβ oligomer, glial activation and oxidative stress are potential therapeutic approaches for AD treatment. We previously found alpha-tocopherol quinine (α-TQ) inhibited Aβ aggregation and cytotoxicity, decreased the release of inflammatory cytokines and reactive oxygen species (ROS) in vitro. However, whether α-TQ ameliorates memory deficits and other neuropathologies in mice or patients with AD remains unknown. In this study, we reported that orally administered α-TQ ameliorated memory impairment in APPswe/PS1dE9 transgenic mice, decreased oxidative stress and the levels of Aβ oligomer in the brains of mice, prevented the production of inducible nitric oxide synthase and inflammatory mediators, such as interleukin-6 and interleukin-1β, and inhibited microglial activation by inhibiting NF-κB signaling pathway. These findings suggest that α-TQ has potential therapeutic value for AD treatment. Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Behavior, Animal; Brain; Disease Models, Animal; Inflammation; Interleukins; Memory Disorders; Mice; Mice, Transgenic; Microglia; NF-kappa B; Oxidative Stress; Signal Transduction; Spatial Memory; Vitamin E | 2016 |