SENS Foundation Funds Research Into a Therapy for TTR Amyloidosis

A condition called TTR amyloidosis - very rare in young people - appears to cause the death of the elderly who survive or evade all of the other common age-related diseases:

TTR is a protein that cradles the thyroid hormone thyroxine and whisks it around the body. In TTR Amyloidosis, the protein amasses in and clogs blood vessels, forcing the heart to work harder and eventually fail. "The same thing that happens in the pipes of an old house happens in your blood vessels"

This is one of many types of amyloid that build up in the body with age. If we want to repair the damage of aging, we'll have to learn how to remove these unwanted substances - and certainly find ways to reverse the course of TTR amyloidosis, which at present looks very much like the roadblock at the end of life. Finding ways to break down amyloids, such as by training the immune system to attack them, is one of the seven research themes of the Strategies for Engineered Negligible Senesence (SENS).

I notice that the SENS Foundation recently announced funding for research into developing a therapy for TTR amyloidosis:

There is already a largely-unrecognized burden of [amyloid]-related morbidity and mortality in the population today, both as a principle cause of death and disease and as a contributor to the total dysfunction of the aging cardiovascular system. And the situation will worsen globally over the course of the next 20 to 50 years, beginning in the industrialized world and the sequentially emerging in China, India, Mexico, the Middle East and beyond; ironically, this will be particularly so to the degree that other diseases are better-managed by progress in conventional medicine, or cured by rejuvenation biotechnology.

These features make the removal of wild-type TTR aggregates [a] key priority for SENS Foundation as a biomedical charity dedicated to accelerating the development of rejuvenation biotechnology. Accordingly, SENS Foundation has had an open request for proposals (RFP) for research toward the development of TTR-clearing therapies for several years now, and has approached several prominent researchers in the genetic amyloidosis field to submit applications for funding. Until recently, however, the Foundation had not received any strong proposals. But thanks to the efforts of [Supercentenarian Research Foundation's] Stan Primmer, such a proposal has recently come together and the Foundation has been given the opportunity to fund it - and I am pleased to have the privilege of announcing that the proposal has been vetted, approved, and funded, and preliminary work will soon be under way.

The first phase of the research is funded to the tune of $150,000, and will involve the development of antibodies that can safely break down TTR amyloid and thus render it harmless.

We are delighted to have such a strong project underway, in the hands of recognized experts in the field, and I am personally grateful for the critical networking done by Primmer and the Supercentenarian Research Foundation to bring the proposal together, and proud of SENS Foundation's role as funder of this promising project. TTR-based senile cardiac amyloidosis is an underdiagnosed and heretofore-untreatable disease that is prevalent in the aging population and poised to become a widespread medical problem with the aging of the global population and the improved treatment of more familiar age-related diseases. We will watch the progress of this latest funded research project with keen anticipation, and look cautiously forward to the ultimate culmination of the preclinical groundwork in a therapy for human patients.

Funding this new research is particularly crafty for SENSF because treating super-centenerians for TTR-amyloidosis provides a nice opportunity to demonstrate maximum lifespan extension in a relatively compressed study time (10-15 years at most). This would make a huge splash since it might break people's set ideas about the "naturalness" & immutability of the current human life-span.

Posted by: Doode at September 24th, 2010 8:42 AM
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