8 replies to this topic

[ihatesnow]

http://sciencenews.o...th_thioflavin_T

[AdamI]

I read more on that study awhile back and it said that it was especially Thioflavin-T that was the best "tagger" of bad proteins.
It was curcumin and Thioflavin-T that they tested, I see that many here on this forum takes curcumin, but why not Thioflavin as well, since it's appearantly alot more potent, according to one study anyway

Is there any tip on where to buy it? Because the only place I could find wanted 120 euro just for the shipping. And then the Thioflavin-T costed 54 euro for 100 grams...

A bit steep shipping cost I think:)

[niner]

Here is a working link to the Science News article.

Here is the abstract of the Nature paper that they're talking about.

And here is a commentary in Rejuvenation Research that is pretty interesting. Scroll down a little for most of text. If you only read one, I'd pick this one.

It's a pretty cool result. Don't forget that they are worms, not mammals. Worms are susceptible to protein homeostasis problems. Also, the worms that showed the biggest result were genetically modified to have severe protein aggregation problems. It's still a very interesting result.

[mpe]

Is Thioflavin related to Methylene Blue ?

[niner]

Thioflavin T
 200px-Thioflavin_T.png   4.76KB   0 downloads


Methylene blue
 220px-Methylene_blue.svg.png   2.52KB   0 downloads

You can see some similarities in the structures. The central tricyclic portion of MB is planar, while the dimethylaminophenyl group in thioflavin is twisted out of plane about 45 degrees. Similarities, but differences too. They aren't really analogs of each other. It's possible that they have some similarity in their behavior toward amyloids.

[mpe]

Thanks Niner

[tunt01]

 

Longevity-promoting superstar gets revealed in Caenorhabditis reproducibility project

 

"The goal of the CITP is to identify pro-longevity chemicals that are effective across diverse genetic distances making them excellent candidates for trials in more complex animals, including mammals," said Gordon Lithgow, PhD, a professor at the Buck Institute for Research on Aging and a senior author of the paper. Lithgow runs the Buck lab that in 2011 showed that Thioflavin T extended lifespan in healthy nematode worms by more than 50 percent and slowed the disease process in worms engineered to mimic aspects of Alzheimer's disease. "Running experiments in three discrete laboratories allowed us to demonstrate the reproducibility of our study with Thioflavin T," he said. "But it's important to note that some of our other compounds did not pass this stringent test - getting feedback on the 'fails' also furthers the larger effort."

CITP researchers from the Buck, Rutgers University and the University of Oregon characterized the lifespans of 22 Caenorhabditis strains spanning three species. Thioflavin T was found to be the most robust pro-longevity chemical, as it extended the lifespan of all strains tested. In addition, researchers found that six out of the ten pro-longevity chemicals significantly extended lifespan in at least one strain of Caenorhabditis. Three dietary restriction mimetics were mainly effective across strains of C. elegans but showed more variable responses in other species. "Nearly 100,000 worms were individually monitored during this initial project," said Mark Lucanic, PhD, a postdoc in the Lithgow lab and first author of the paper. "We hope that the scope and focus of this project will give confidence that our consortium can identify promising compounds for further testing on aging."

 

 

Read more at: https://medicalxpres...bditis.html#jCp

 

 

Nature paper:  http://www.nature.co...les/ncomms14256

 

I have no clue how to bridge the dosage levels in a c. elegan to a mammal/human. I also am not aware of any mammal models that validate Thioflavin T.

 

 

Edited by prophets, 24 February 2017 - 03:45 AM.

[AdamI]

 

 

Cool, well hopefully we will get to know more of the study.

Does anyone sell this yet?

[tunt01]

If anyone has access to a copy of this paper, I'd like to see it.

 

 

Oral Administration of Thioflavin T Prevents Beta Amyloid Plaque Formation in Double Transgenic AD Mice

 

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the fourth leading cause of death in the United States and most common cause of adult-onset dementia. The major hallmarks of AD are the formation of senile amyloid plaques made of beta amyloid and neurofibrillary tangles (NFT) which are primarily composed of phosphorylated tau protein. Although numerous agents have been considered as providing protection against AD, identification of potential agents with neuroprotective ability is limited. Thioflavin T has been used in the past to stain amyloid beta plaques in brain. In this study, Thioflavin T (ThT) and vehicle (infant formula) were administered orally by gavage to transgenic (B6C3 APP PS1; AD-Tg) mice beginning at 4 months age and continuing until sacrifice at 9 months of age at 40mg/kg dose. The number of amyloid plaques was reduced dramatically by ThT treatment in both male and female transgenic mice compared to those in control mice. Additionally, GFAP and Amylo-Glo labeling suggest that astrocytic hypertrophy is minimized in ThT-treated animals. Similarly, CD68 labeling, which detects activated microglia, along with Amylo-Glo labeling, suggests that microglial activation is significantly less in ThT-treated mice. Both Aβ-40 and Aβ-42 concentrations in blood rose significantly in the ThT-treated animals suggesting that ThT may inhibit the deposition, degradation, and/or clearance of Aβ plaques in brain.