Showing posts with label neuroinflammation. Show all posts
Showing posts with label neuroinflammation. Show all posts

Tuesday, October 9, 2018

Researchers Have Been Able To See Neuroinflammation Of Alzheimer's By Studying Dish Model!



"Building on their development of the first culture system to replicate fully the pathology behind Alzheimer’s disease, a Massachusetts General Hospital (MGH) research team has now produced a system that includes neuroinflammation, the key biological response that leads to the death of brain cells." Read article...

Alzheimer’s in a dish’ model provides some answers. The Harvard Gazette. July 31, 2018.



Tuesday, August 7, 2018

Berries Improve Gut Health and are Protective Against Neuroinflammation!





Experts believe that gut dysbiosis is a cause of environmental illness. Changes in the gut biome can be caused by antibiotic use, environmental insults from chemicals in food and water and high fat and high sugar diets. These changes lead to morphological changes in the wall of the intestines that allows for easier translocation of harmful bacteria. It is believed that translocation may be one significant cause of chronic fatigue syndrome. In addition, it is believed that dysbiosis may lead to neuroinflammation that is believed to be a major source of symptoms in chronic fatigue and fibromyalgia.

Numerous studies published in the recent past have shown that consumption of some fruits and herbs may improve gut health. Research has demonstrated that anthocyanins in berries may counteract dysbiosis. In addition, they also have anti-neuroinflammatory properties and allow for better communication between the gut and the brain. Lastly, they alter tryptophan metabolism increasing the neuroprotective metabolite kynurenic acid. (1) Incidentally, this pathway also produces the antioxidant 3-hydroxyanthranilic acid which inhibits inflammatory proteins by activating Nrf2. (2) 





1. Gut microbiota modulation accounts for the neuroprotective properties of anthocyanins. Scientific reports, Vol. 8, No. 1. (27 July 2018) by Cláudia Marques, Iva Fernandes, Manuela Meireles, et al.

2. 3-Hydroxyanthranilic acid, one of L-tryptophan metabolites, inhibits monocyte chemoattractant protein-1 secretion and vascular cell adhesion molecule-1 expression via heme oxygenase-1 induction in human umbilical vein endothelial cells. Atherosclerosis, Vol. 187, No. 2. (August 2006), pp. 274-284 by Hyun-Ock O. Pae, Gi-Su S. Oh, Bok-Soo S. Lee, et al.


Saturday, August 4, 2018

Fire Ant Pesticide Causes Neuroinflammation, Depression of the Natural Antioxidant System and Anxiety!




Bifenthrin is a pesticide that has commercial use for fire ants. Fire ants are a health and safety concern in many southern states of the U.S and there are over 200 species of fire ants spread out around the world. There venom is toxic and their bites can lead to allergic reactions and anaphylaxis in some people and animals. (1)

In the U.S., bifenthrin use is strictly labeled for the eradication of fire ants. As far as I know, there is no other use of it that is on label here in the US but is used extensively for agricultural use in other countries. In the past, the use of the chemical has been associated with the development of neurological disease and symptoms of anxiety. However, the mechanism of how it acts on the brain was not known.  In a recent study, it was demonstrated that rats exhibited anxiety after 60 of treatment with the chemical. In addition, it was discovered that these rats had extensive oxidation of lipids in two centers of the brain. Also, there was a decrease in glutathione and anti-oxidant activity and increased levels of oxidative stress and Tnf-a and reduced Nrf2. This is an important study in that it demonstrates how pesticides act on areas of the brain to cause neuroinflammation through activities of Nrf2/NF-kb pathway to promote anxiety. (2)


Wipedia. https://en.wikipedia.org/wiki/Bifenthrin


Inflammatory and oxidative mechanisms potentiate bifenthrin-induced neurological alterations and anxiety-like behavior in adult rats. Toxicology letters, Vol. 294 (15 September 2018), pp. 73-86 by Brahim Gargouri, Harsharan S. Bhatia, Michèle Bouchard, Bernd L. Fiebich, Hamadi Fetoui http://www.citeulike.org/user/kimberlykramer2015/article/14622148

Monday, July 30, 2018

Bipolar and Depression Could Be Caused by Dysregulation in the Body's Antioxidant System




"Although bipolar disorder and depression are not found at this time in the NRF2 diseasome, it is becoming evident that they exhibit neuroinflammatory and degenerative pathophenotypes that at least in mouse models imply deregulation of NRF2". 

         Systems Medicine Approach to NRF2 in Chronic Diseases 375. NRF2 (Martin-de-Saavedra et al., 2013; Freitas et              al., 2016; Yao et al., 2016).

Thursday, April 2, 2015

TLR4 Activity in the Gut Contributes to Symptoms in Chronic Fatigue Syndrome!


"Interactions between gut microorganisms and host immune function have been shown to contribute to aberrant inflammation in CFS/ME patients. Commensal and/or pathogen-associated molecular patterns detected by Toll-like receptors (TLRs) expressed on intestinal epithelial cells appear to trigger inflammatory signaling cascade leading to neuroinflammation and neurodegeneration."

The Role of Toll-like Receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: A New Promising Therapeutic Approach? CNS & neurological disorders drug targets (25 March 2015) by M. E. Gambuzza, F. M. Salmeri, L. Soraci, et al.  http://www.citeulike.org/user/kimberlykramer2015/article/13568646


For further reading:
Infection/Endotoxin in Chronic Fatigue, Fibromyalgia and Multiple Chemical Sensitivity.