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Australian researchers are one step closer to find a new treatment for multiple sclerosis (MS) that may be able to reverse the effects the disease has on the brain.

Researches from Monash University in Melbourne believe they can achieve the results by using an old drug called Ditpa.

When the drug was trialled on mice, the paralysed animals were able to walk again.

“We don’t have any drugs that are available at the moment that can enhance the repair mechanism that this drug is purported to do,” Dr Steve Petratos from Monash University told 7NEWS.

MS, a condition of the central nervous system, interferes with nerve impulses in the brain, causing muscle spasms, weakness, balance problems and fatigue.

For people like 31-year-old mother Lauren Hunt, just sitting at a desk can be excruciating.

“Muscle weakness, nerve pain, muscle pain, all those things are battles for me every day,” Hunt, who was diagnosed six years ago, said.


There’s no cure for MS, but this new treatment gives hope to sufferers.

“That would be a dream come true for all of us and everyone else living with MS and these constant worries especially as a parent,” Hunt said.

“With MS, this drug could have profound outcomes in quality of life for individual patients,” Petratos added.

The research team now needs $2 million to get the drug ready for human clinical trials, which could happen within three to five years.

https://actrims.confex.com/actrims/2016 ... %20LEE.pdf

There is a 2016 ACTRIMS poster about DITPA...so is this really a new breakthrough? Why so slow to human trial? Would it cause systemic mayhem in people who don’t need it for thyroid-related issues?

Questions!! Dontchya wish there was someone who could/would actually (correctly) answer all your questions? It would probably be heaven and hell at the same time. What a mind bender to contemplate!

Oligodendroglial Lineage Cells in Thyroid Hormone-Deprived Conditions.
Stem Cells Int. 2019 Apr 30

• Oligodendrocytes are supporting glial cells that ensure the metabolism and homeostasis of neurons with specific synaptic axoglial interactions in the central nervous system. These require key myelinating glial trophic signals important for growth and metabolism. Thyroid hormone (TH) is one such trophic signal that regulates oligodendrocyte maturation, myelination, and oligodendroglial synaptic dynamics via either genomic or nongenomic pathways. The intracellular and extracellular transport of TH is facilitated by a specific transmembrane transporter known as the monocarboxylate transporter 8 (MCT8). Dysfunction of the MCT8 due to mutation, inhibition, or downregulation during brain development leads to inherited hypomyelination, which manifests as psychomotor retardation in the X-linked inherited Allan-Herndon-Dudley syndrome (AHDS). In particular, oligodendroglial-specific MCT8 deficiency may restrict the intracellular T3 availability, culminating in deficient metabolic communication between the oligodendrocytes and the neurons they ensheath, potentially promulgating neurodegenerative adult diseases such as multiple sclerosis (MS). Based on the therapeutic effects exhibited by TH in various preclinical studies, particularly related to its remyelinating potential, TH has now entered the initial stages of a clinical trial to test the therapeutic efficacy in relapsing-remitting MS patients (NCT02506751). However, TH analogs, such as DITPA or Triac, may well serve as future therapeutic options to rescue mature oligodendrocytes and/or promote oligodendrocyte precursor cell differentiation in an environment of MCT8 deficiency within the CNS. This review outlines the therapeutic strategies to overcome the differentiation blockade of oligodendrocyte precursors and maintain mature axoglial interactions in TH-deprived conditions.
  
  
  

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Oh look, they cured eae. Again. What is this, 300, 499 cures for mice. How many work on people? Oh, 0? Maybe they should look in a different direction.