New Clinical Trial for Mild-Mod AD using ALS & FTD drug

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NF52
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New Clinical Trial for Mild-Mod AD using ALS & FTD drug

Postby NF52 » Sat Jan 12, 2019 7:48 am

For those of you with loved ones diagnosed with mild-moderate AD, there is a new clinical trial that may be of interest. T2 Protect AD. The link provided has specifics about the 48 week program, and an interactive map so you can see where the 30 study sites will be (I would require such a map for every clinical trial if I could!)
T2 Protect AD is a clinical trial testing the investigational drug troriluzole in people with mild to moderate Alzheimer’s disease (AD).The study is designed to determine if troriluzole can protect against, slow down, and potentially improve memory and thinking problems that increase as Alzheimer’s disease progresses.

Here's a reader-friendly source for info about the clinical trial:
https://www.sciencealert.com/researchers-are-testing-if-asl-drug-can-also-halt-alzheimer-s-memory-loss

Looks like this study targets a protein called TDP-43. This is a new and promising target for AD research, since it's been known since 2006 to be a key player in both frontal-temporal dementia and ALS. This study uses a new drug troriluzole, a version of a drug, riluzole, that has been approved since 1995 for the treatment of ALS.
Here's a quote from the ALZ Forum:
In 2006, TAR DNA-binding protein 43 (TDP-43) was identified as the cardinal protein in the most common subtypes of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). TDP-43 is a widely expressed nuclear protein that binds both DNA and RNA [and] helps regulate many aspects of RNA processing... TDP-43 affects RNAs that encode proteins involved in autophagy and other cellular protein homeostasis and clearance pathways. A role in axonal transport has also been proposed. In neurodegenerative diseases, neuronal and glial TDP-43 becomes mislocalized to the cytoplasm, where it aggregates into stress granules and insoluble inclusion bodies. These inclusions occur...in about a quarter of Alzheimer’s disease cases. Regardless of the proximal cause of a given patient’s disease, distribution of TDP-43 pathology tends to correlate with brain areas of atrophy and the stage of dementia, hence TDP-43 dysregulation is considered to reflect a common downstream mechanism of neurodegeneration.
[Emphasis added.] https://www.alzforum.org/alzpedia/tdp-43
4/4 and still an optimist!

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