Posted From: 18.104.22.168
|Posted on Monday, July 21, 2008 - 5:13 pm: || |
Rapid Alzheimer's Improvement After New Immune-based Treatment
It works by inhibiting TNF-alpha (tumor necrosis factor). I did a search on TNF-alpha + glutamate, and this is one of the first articles that came up:
Posted From: 22.214.171.124
|Posted on Monday, July 21, 2008 - 5:21 pm: || |
A new Alzheimer's hypothesis: Dysfunctional calcium channels in the brain
|Posted on Tuesday, July 22, 2008 - 1:48 pm: || |
Jennifer, Very interesting, thanks. One sentence from the nih website. "These data indicate that TNF alpha and glutamate can act synergistically to induce neuronal cell death."
I'm very interested in these studies, being that my dad had early onset Alzheimer's and my mother had some type of dementia in her early 90s.
Posted From: 126.96.36.199
|Posted on Monday, November 10, 2008 - 1:00 pm: || |
This article says that amalyoid-B (sp) plaques attack the mitochondria, causing them to rupture and die. There's a mouse variety that lacks a protein involved with mitochondrial pores, which - keeps them from bursting due to an influx of calcium. That sounds familiar - I think Dr. Blaylock described that as how glutamate kills neurons.
Now let's see what happens when I google the protein:
Cyclophilin D, which is located in the matrix of mitochondria, is a component of the mitochondrial permeability transition pore. The pore opening raises the permeability of the mitochondrial inner membrane, allows influx of cytosolic molecules into the mitochondrial matrix, increases the matrix volume, and disrupts the mitochondrial outer membrane. As a result, the mitochondria fall into a functional disorder, so the opening of the pore plays an important role in cell death. Cyclophilin D is thought to regulate the opening of the pore because cyclosporin A, which binds to CyP-D, inhibits the pore opening.
Now for my favorite game...
I found a bunch of links that mention glutamate, but there's no direct link...
This link seems to imply that Cyclophilin D causes increased sensitivity to excess calcium.
And this is closer....I believe, if I read it correctly, that glutamate was used to induce calcium concentrations to rise, and therefore damage mitochondria.
It's plausible that folks with "too much" Cyclophilin D would me more sensitive to glutamate and other substances that increase calcium in the cells. But I don't think glutamate directly effects Cyclophilin D.
MSG kills indeed. Um, is anyone familiar with cyclosporin A?
|Posted on Monday, November 10, 2008 - 2:02 pm: || |
Here is some more info about TNF-alpha and Alzheimers:
|Posted on Wednesday, November 12, 2008 - 11:12 am: || |
|Posted on Wednesday, November 12, 2008 - 2:26 pm: || |
Vitamins...we get a lot of email and inquiries here concerning them. Many would like to be able to take a simple single pill that wouldn't bother them. www.needs.com just sent me another pamphlet and they had an article about Vitamin Code vitamins. It was interesting reading about how they are produced. They are in veggie gelcaps, but the "raw" vitamins without fillers, could be removed from them. Wanted to know what you guys thought...google them using Vitamin Code vitamins..they seem like a new product. Ingredients can be found at most of the sites.
|Posted on Sunday, January 18, 2009 - 10:33 am: || |
This is an interesting article that offers some tantalizing clues as to the origin of Alzheimer's. A single gene was discovered to regulate pain, then later memory and learning. A generalization can be made that pain reduces brain function - I know that was true for me. I used to marvel at how many more things my brain could store -
"Studies published in mid 2008 suggest that the devastating condition may be related to Calcium regulation gone awry. The accumulation of amyloid plaques in brain cells, usually blamed for Alzheimer’s, might be a consequence of the Calcium-imbalance rather than the culprit for the disease.
And Calcium regulation is also responsible for tuning the activity of the DREAM-gene. Calcium homeostasis may thus be the link between pain perception, learning and memory. "
Calcium regulation screwed up? I wonder if perhaps excitotoxins that act on calcium channels counts as one way to screw up calcium regulation. I think I posted something about that recently, namely that there's a condition or gene that makes one more susceptible to glutamate -
|Deb A. |
|Posted on Monday, January 19, 2009 - 4:36 pm: || |
Jennifer, I think you need to write a book with all the research you have been compiling...no kidding.
|Posted on Monday, May 24, 2010 - 7:53 am: || |
Titled "New Path for Alzheimer's Therapies".
Here's the relevant part:
"The novelty lies in a new mechanism through which the amyloid peptide, the major pathogen in Alzheimer's disease, provokes neuronal death. The Basque researchers have found that this peptide activates some receptors that lead cells to overexcitation and subsequent death;"
Though I'm not sure how they can call it a new mechanism. Sounds like amyloid does what MSG does. Though glutamate is not mentioned in this article, but it is in the actual study title.