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Dietary lycopene supplementation improves cognitive performances in tau transgenic mice expressing P301L mutation via inhibiting oxidative stress and tau hyperphosphorylation

Bibliographic

Year of Publication:
2017
Contact PI Name:
Yan Hong
Contact PI Affiliation:
Department of Nutrition, Tianjin Institute of Health and Environmental Medicine, Tianjin, China
Co-Authors:
Lixia Yu, Weiguang Wang, Wei Pang, Zhonghai Xiao, Yugang Jiang
Primary Reference (PubMED ID):
Funding Source:
Nutrition and Science Foundation of BY-HEALTH Co. Ltd.
Tianjin Research Program of Application Foundation and Advanced Technology
Study Goal and Principal Findings:

Background: Oxidative stress is implicated in the pathogenesis of Alzheimer’s disease (AD) and other tauopathies and participates in their development by promoting hyperphosphorylation of microtubule-associated protein tau. Lycopene, as an effective antioxidant, combined with vitamin E seemed to be additive against oxidative stress.

Objective: The present study was undertaken to examine whether lycopene or lycopene/vitamin E could exert protective effects on memory deficit and oxidative stress in tau transgenic mice expressing P301L mutation.

Materials and methods: P301L transgenic mice were assigned to three groups: P301L group (P301L), P301L+lycopene (Lyc), and P301L+lycopene/vitamin E (Lyc+VE). Age-matched C57BL/6J mice as wild type controls (Con) were used in the present study. Spatial memory was assessed by radial arm while passive memories were evaluated by step-down and step-through tests. Levels of tau phosphorylation were detected by western blot. Oxidative stress biomarkers were measured in the serum using biochemical assay kits.

Results: Compared with the control group, P301L mice displayed significant spatial and passive memory impairments, elevated malondialdehyde (MDA) levels and decreased glutathione peroxidase (GSH-Px) activities in serum, and increased tau phosphorylation at Thr231/Ser235, Ser262, and Ser396 in brain. Supplementations of lycopene or lycopene/vitamin E could significantly ameliorate the memory deficits, observably decreased MDA concentrations and increased GSH-Px activities, and markedly attenuated tau hyperphosphorylation at multiple AD-related sites.

Conclusions: Our findings indicated that the combination of lycopene and vitamin E antioxidants acted in a synergistic fashion to bring significant effects against oxidative stress in tauopathies.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Dietary Interventions & Supplements
Therapeutic Agent:
Lycopene
Therapeutic Target:
Multi Target
Therapy Type:
Dietary Interventions & Supplements
Therapeutic Agent:
Vitamin E
Therapeutic Target:
Multi Target

Animal Model

Model Information:
Species:
Mouse
Model Type:
Tau
Strain/Genetic Background:
Not Reported

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest

Outcomes

Outcome Measured
Outcome Parameters
Behavioral
Passive Avoidance Test
Radial Arm Maze
Biochemical
Glutathione Peroxidase (GPx)
Malondialdehyde (MDA)
Superoxide Dismutase (SOD)
phospho-Tau
phospho-Tau/Total Tau Protein
Total Tau Protein
Toxicology
Body Weight
Food Intake