International Journal of Clinical Nutrition & Dietetics Volume 5 (2019), Article ID 5:IJCND-139, 5 pages
Research Article
Neuroprotection Afforded by a Preventive CogniXtra Treatment Against Amyloid Beta Aβ25-35 Peptide-induced Toxicity in Mice

Guillaume Blivet1, Francois J. Roman2*, Johann Meunier2, Laura Ceolin2, Jean-Marie Butterlin3 and Jacques Touchon4,5,6

1Montpellier, France
2Amylgen, Montferrier-sur-Lez, France
3Health Optimisation Devices B.V., Maastricht, Netherlands
4INSERM U1061, Montpellier, France
5Montpellier University, Montpellier, France
6JT Conseils, Montpellier, France
Dr. François J. Roman, Amylgen, 2196, Agropolis 2, boulevard de La Lironde, 34980 Montferrier-sur-Lez, France, Tel: +33 (0)610231475; E-mail:
08 November 2018; 04 February 2019; 06 February 2019
Blivet G, Roman FJ, Meunier J, Ceolin L, Butterlin JM, et al. (2019) Neuroprotection Afforded by a Preventive CogniXtra Treatment Against Amyloid Beta Aβ25-35 Peptide-induced Toxicity in Mice. Int J Clin Nutr Diet 5: 139. doi:
This work was funded by Health Optimisation Devices B.V., Maastricht, Netherlands.


Objective: A number of encouraging research studies have shown the importance of nutritional approach in order to protect the brainhealth. Here we present the efficacy of a daily administration of a unique complex combination of omega 3 fatty acids and antioxidants (cogniXtra) as a neuroprotective treatment on early symptoms of Alzheimer’s disease (AD) mouse model.
Methods: Mice were treated per os once a day with various combinations of dacosahexaenoic acid (DHA), glutathione (GSH), phosphatidylcholine (PC), curcumin (CUR) and resveratrol (RES) including the special combination cogniXtra (GSH + PC+ CUR + RES + DHA) starting 20 days before and until10 days after the onset of the neurotoxicity induced by a central injection of amyloid-beta 25-35 (Aβ25-35)- oligomeric peptide. Protection against the neurotoxicity of Aβ25-35 was assessed carrying out two behavior tests evaluating short-term memory (Y-maze) and long term memory (step through passive avoidance test-STPA) and the measurement of a key brain biomarker, lipid peroxidation (LPO).
Results: Our present research demonstrates the importance of a correct association of different substances whereas the treatment with each of them alone was unable to provide any protection from the toxic effects produced by Aβ25-35 injection. CogniXtra formulation combining all of the components was the only one able to fully reverse all the memory deficits both in the Y-maze and in the STPA tests and also to completely protect from oxidative stress as demonstrated by the important LPO elevation measured in the hippocampus.
Conclusion: This study indicates that acombination treatment (cogniXtra) administration for thirty consecutive days produces a complete neuroprotective effect on the neurotoxic events produced by Aβ25-35 oligomeric peptide injection. The efficacy of a preventive treatment with cogniXtrain this preclinical model is similar to what could be achieved with other pharmacological approaches. These results strongly suggest the therapeutic interest of cogniXtra for the preventive treatment of AD.