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3 mai 2011 2 03 /05 /mai /2011 09:58

 

 

Dr. Bickford (University of South Florida) a montré que la Spiruline :

                Réduit le dommage anoxique de 70% en cas d'AVC.

                Réduit la dégénérescence cérébrale chez les animaux âgés. 

                Améliore la récupération des neurones à Dopamine.

                Procure une neuro protection pour la souffrance cellulaire des neurones moteurs. 


 

New Research on Spirulina for Brain Health plus the First Published Human Clinical Trial on Astaxanthin for Brain Health

Neurodegenerative diseases are one of the fastest growing areas of health concerns for today’s health practitioners; for example, there are no known cures for Alzheimer’s or senility, both of which are becoming prevalent as the world’s population ages.

Fortunately, both Spirulina and Astaxanthin have shown great promise as potential aids in the prevention of age-related dementia.

Spirulina: Dr. Paula Bickford of the University of South Florida is one of the most respected researchers on age-related neurological issues. She has held a variety of leadership positions in her field, and now serves as President of the American Society for Neural Therapy and Repair. Dr. Bickford had been responsible for a great deal of the research showing health benefits for blueberries, which subsequently led to a huge increase in blueberry consumption. But over the last few years, Dr. Bickford has turned her sights to Spirulina as a potent neuroprotective agent. In a series of four rodent studies, Dr. Bickford found that Spirulina:

                Reduced brain damage from strokes by 70%

                Reduced degeneration of the brains of aging animals

                Enhanced dopamine neuron recovery

                Gives neuroprotective support for dying motor neurons

The last of these studies was of particular interest in that the research led Dr. Bickford’s Team to conclude that “A Spirulina supplemented diet may be a potential alternative or adjunctive treatment for ALS [Amiotrophic Lateral Sclerosis or ‘Lou Gehrig’s Disease,’ an incurable, fatal neurodegenerative condition].”

Astaxanthin: There have also been several animal research models showing that Astaxanthin serves to protect the brain and potentially improve memory in rodents. One of these studies concluded “The current result indicates that Astaxanthin may have beneficial effects in improving memory in vascular dementia.” It appears that Astaxanthin actually made the mice in this study smarter!

Fortunately, there is now a human clinical trial on thirty middle-aged and senior subjects which corroborates these animal study results. In this groundbreaking study, the superior antioxidant status of Astaxanthin was hypothesized to be the mechanism of action, and the researchers concluded that Astaxanthin may help prevent dementia.

With the huge increase in PR and press coverage of both Astaxanthin and Spirulina, the time is now to launch a brain health supplement featuring these nutrients. For more information on the research referenced above or to discuss formulation ideas, please e-mail us at bcapelli@cyanotech.com or call 808.334.9415.

 

Int Immunopharmacol. 2010 Dec;10(12):1560-72. Epub 2010 Oct 15.

Down-regulation of IL-6 production by astaxanthin via ERK-, MSK-, and NF-κB-mediated signals in activated microglia.

Source

Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, Repulic of Korea. yeonhkim@yonsei.ac.kr

In this study, we investigated the effect of astaxanthin on IL-6 in activated microglial cells because excessive interleukin-6 (IL-6) production by activated brain microglia has been linked to many neurological disorders and proper regulation of IL-6 is critical for maintaining brain homeostasis. Astaxanthin inhibited lipopolysaccharide (LPS)-stimulated IL-6 mRNA and protein in BV-2 microglial cells. Moreover, LPS-induced p-IKKα, p-IκBα, and p-NF-κB p65 levels were all suppressed by astaxanthin. The translocation of p-NF-κB p65 from the cytosol into the nucleus and transcriptional activity were inhibited by astaxanthin. IL-6 expression and NF-κB transcriptional activation were inhibited by astaxanthin, as well as inhibitors of NF-κB and MAPK in LPS-stimulated BV-2 microglial cells. Consistent with these findings, astaxanthin down-regulated the activation of p-extracellular signal-regulated kinase 1/2 (p-ERK1/2) and p-mitogen- and stress-activated protein kinase 1(p-MSK1), but not of p-c-jun N-terminal kinase (p-JNK). Astaxathin also decreased IL-6 mRNA and protein levels in LPS-stimulated primary microglial cells, RAW264.7 macrophages, and peritoneal macrophages. In addition, IL-6 suppression through astaxanthin-induced down-regulation of p-ERK1/2, p-MSK1, and p-NF-κB p65 occurred in microglial cells stimulated with LPS or stromal derived factor (SDF)-1α. Astaxathin also inhibited the secretion and mRNA expression of IL-6 in SDF-1α-stimulated microglial cells. SDF-1α-stimulated ERK1/2, MSK1, and NF-κB p65 phosphorylation were reduced by astaxanthin. Therefore, our results suggest that astaxanthin regulates IL-6 production through a p-ERK1/2-MSK-1- and p-NF-κB p65-dependent pathway in activated microglial cells.

Copyright © 2010 Elsevier B.V. All rights reserved.

PMID:
 
20932499
 
[PubMed - indexed for MEDLINE]

Phys Chem Chem Phys. 2010 Jan 7;12(1):193-200. Epub 2009 Nov 6.

Carotenoids can act as antioxidants by oxidizing the superoxide radical anion.

Source

Departamento de Química, División de Ciencias Básicas e Ingeniería, Universidad Autónoma Metropolitana-Iztapalapa, San Rafael Atlixco 186, Col. Vicentina, Iztapalapa. AP POSTAL 55-534, México DF 09340, México.

 

The electron transfer (ET) reaction between carotenoids and the superoxide radical anion is found to be not only a viable process but also a very unique one. The nature of the O(2) (-) inverts the direction of the transfer, with respect to ET involving other ROS: the O(2) (-) becomes the electron donor and carotenoids (CAR) the electron acceptor. Therefore the "antioxidant" activity of CAR when reacting with O(2) (-) lies in their capacity to prevent the formation of oxidant ROS. This peculiar charge transfer is energetically feasible in non-polar environments but not in polar media. In addition the relative reactivity of CAR towards O(2) (-) is drastically different from their reactivity to other ROS. Asthaxanthin (ASTA) is predicted to be a better O(2) (-) quencher than LYC and the other CAR. The CAR + O(2) (-) reactions were found to be diffusion controlled. The agreement with available experimental data supports the density functional theory results from the present work.

PMID:
 
20024459
 
[PubMed - indexed for MEDLINE]


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