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Clinical trials for FTD and AD
SunnyCA
Posted: Thursday, May 16, 2013 11:28 AM
Joined: 2/14/2012
Posts: 1752


Remember Rember?  It made a huge splash five years ago ... and then just disappeared.

 

Well, it's back, in a new and improved form. See:

http://www.alzforum.org/new/detail.asp?id=3283

 

 And it's heading into three Phase III clinical trials.  Some of the sites have already started recruiting.

 

http://clinicaltrial.gov/ct2/show/study/NCT01689233
Safety and Efficacy Study Evaluating TRx0237 in Subjects With Mild Alzheimer's Disease
Accepting patients up to 89 years old (no lower age limit)

http://clinicaltrial.gov/ct2/show/NCT01689246
Safety and Efficacy Study Evaluating TRx0237 in Subjects With Mild to Moderate Alzheimer's Disease
Accepting patients up to 89 years old (no lower age limit)

http://clinicaltrial.gov/ct2/show/NCT01626378
Safety and Efficacy Study Evaluating TRx0237 in Subjects With Behavioral Variant Frontotemporal Dementia (bvFTD)
Accepting patients up to 69 years old


Lane Simonian
Posted: Thursday, May 16, 2013 12:42 PM
Joined: 12/12/2011
Posts: 4782


If Rember (methylene blue) works for Alzheimer's disesae, it likely works by blocking inducible nitric oxide production. 

 

Both the induction of iNOS from the stress of saline injections and LPS were completely eliminated by MB indicating that MB might be beneficial in preventing injury to brain tissue following LPS injection. 

 

If you block the production of inducible nitric oxides, you block the production of peroxynitrites, and if you block the production of peroxynitrites, you block almost every aspect of Alzheimer's disease including the target of Rember--the aggregation of tau proteins. 

 

Brains from subjects who have Alzheimer's disease (AD) express inducible nitric oxide synthase (iNOS). We tested the hypothesis that iNOS contributes to AD pathogenesis. Immunoreactive iNOS was detected in brains of mice with AD-like disease resulting from transgenic expression of mutant human β-amyloid precursor protein (hAPP) and presenilin-1 (hPS1). We bred hAPP-, hPS1-double transgenic mice to be iNOS+/+ or iNOS/, and compared them with a congenic WT strain. Deficiency of iNOS substantially protected the AD-like mice from premature mortality, cerebral plaque formation, increased β-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of β-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213235/ 

 

To investigate the upstream effector that led to tau hyperphosphorylation, nitration, and accumulation as seen in Alzheimer's disease brain, and the underlying mechanisms, we bilaterally injected SIN-1, a recognized peroxynitrite donor, into the hippocampus of rat brain. We observed that the level of nitrated and hyperphosphorylated tau was markedly increased in rat hippocampus 24 h after drug administration, and these alterations were prevented by preinjection of uric acid, a natural scavenger of peroxynitrite.

 

http://www.ncbi.nlm.nih.gov/pubmed/16816118 

 

Once you understand the cause of a disease, it becomes much easier to treat.


Myriam
Posted: Thursday, May 16, 2013 3:06 PM
Joined: 12/6/2011
Posts: 3326


So bummed none of the locations of the trials are in Seattle!