research reports and media, page-3729

Completely agree. I am trying to get something happening for Huntington's Disease (HD) by annoying people with emails and posts, even if it's just a mouse trial. HD is an orphan disease, and we know orphan drugs are popular with big pharma these days. There are currently no good therapeutic treatments for suffers of HD.

I've volunteered with sufferers of HD. It doesn't discriminate against age, race, or healthiness. Once you become symptomatic, you will experience any number of cognitive or motor issues as different parts of the brain die off. I've seen people fully mobile, but can't speak. And people who are 100% there mentally, but confined to wheelchairs and have involuntary movement. Don't even get me started on Juvenile Onset Huntington's Disease (JHD), which is a form of HD that affects children and teenagers.

Based on my amateur research, there are studies that indicate the NF-kB pathway may play a role in the pathogenesis of HD. NF-kB activation is increased in the brains of HD patients and animal models of the disease, which can induce the expression of various pro-inflammatory cytokines and chemokines, contributing to the inflammatory response observed in HD. The relevance to Paradigm is that iPPS has been demonstrated to have anti-inflammatory effects and inhibit the activation of NF-kB.

However, in order for a drug to be effective in treating a neurological disorder like HD, it must be able to cross the blood-brain barrier (BBB) and reach the brain.The BBB is a protective barrier that surrounds the brain and prevents the entry of many molecules, including drugs. There is some research suggesting that combining PPS with the amino acid arginine could help PPS cross the BBB.

Arginine is an amino acid that has been shown to increase blood flow to the brain and enhance the transport of molecules across the BBB. Based on my dodgy science, it seems that iPPS in combination with an off the shelf injectable version of arginine, such as L-Arginine, could potentially enable PPS to cross the BBB, and inhibit NF-kB activation in sufferers of HD.

This would potentially have therapeutic benefits by reducing inflammation in the striatum, which is a part of the basal ganglia involved in motor control and cognitive processing, which is severely affected by HD.Considering both iPPS and L-Arginine are already considered safe, it seems like a no brainer to me to pursue a pre-clinical study of some kind. Hell I will start fundraising if someone can tell me how much it costs to carry out a full study on mice?

I think the potential given what it is doing for suffers of OA is really promising as a potential therapeutic treatment for HD. I am now also posting about in on HC, so that if even just one major shareholder sees it, they might mention it into the ear of someone that may actually get it some more attention. HD needs more attention, being an orphan disease means it's not even on the radar of most people, but it's genuinely a horrible disease. Guess it's similar to Rhett syndrome, in the sense that most people had probably never heard of until Neuren got FDA approval for an orphan drug.