CPHPC and Amyloidosis
Centenarians get to be centenarians by surviving or not suffering the diseases that kill everyone else. So what kills centenarians? This isn't an academic question, as we'd like to engineer a future in which none of us suffer the major diseases of aging, and all of us make it past a century in good health. Understanding the processes that slay those who survive everything else the failing body can throw at us is just as essential to the future of longevity medicine as curing cancer and repairing mitochondria.
If forced to make an educated guess today, I'd have to say that the best evidence is for amyloidosis to be the killer of the oldest old - a buildup of metabolic byproducts that eventually clogs the body's systems to the point of failure. The Supercentenarian Research Foundation outlines some of the case for that conclusion:
Coles argues [that supercentenarians] aren't perishing from the typical scourges of old age, such as cancer, heart disease, stroke, and Alzheimer's Disease. What kills most of them, he says, is a condition, extremely rare among younger people, called senile cardiac TTR Amyloidosis. 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," says Coles.
Folk from the Biogerontology Research Foundation (formed "to support the application of our knowledge of the mechanisms of ageing to the relief of disability, suffering and disease in old age") were kind enough to direct my attention today to a recent update from the amyloidosis research community:
Prof Pepys’s persistence pays off
Amyloidosis is caused by the build up of abnormal "amyloid" proteins in body tissues. Prof Pepys has long believed that the key to understanding the disease is a related blood protein called SAP, which sticks to amyloid fibres and stops enzymes removing them.The FT has covered his work several times. My predecessor David Fishlock described in 1990 Prof Pepys’s discovery of a way to image SAP and amyloid fibres. I wrote in 1995 and 2002 about progress in developing a drug called CPHPC, which aimed to clear the destructive amyloid deposits from patients by removing the protective SAP from their blood.
Prof Pepys was working then in collaboration with Roche. But the Swiss pharmaceutical giant eventually pulled out.
"While we had promising early results [with CPHPC] they were not enough to benefit patients with advanced disease," he says. "Something more dramatic is needed."
That something turns out to a combination of CPHPC with an antibody - a molecular guidance system designed to seek out amyloid deposits in vital organs.
Now Prof Pepys has reached an agreement with another big pharmaceutical group, UK-based GlaxoSmithKline, to collaborate on producing a treatment for amyloidosis based on the CPHPC-antibody combination.
Those of us interested in progress towards the tools needed to remove or repair changes in our tissues that accumulate with age should follow amyloidosis research with interest. Some fraction of the degenerations of aging is caused by just this sort of buildup of unwanted chemical aggregates. Strategies under development for dealing with specific aggregates may turn out be more broadly applicable to future engineered longevity therapies.
Wow, that's interesting. I wonder what the typical lifespan of a centenarian might be if this problem were solved, even in the absence of other cures. An extra year? An extra five? More?
Coles argues [that supercentenarians] aren't perishing from the typical scourges of old age, such as cancer, heart disease, stroke, and Alzheimer's Disease. What kills most of them, he says, is a condition, extremely rare among younger people, called senile cardiac TTR Amyloidosis. 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," says Coles.
Does it meant that the built up of T4 will increase the potential for one to acquire Alzheimer ?
Excuse me if I am confusing a few ideas from my earlier phases of longevity interest, but two ideas jump out to me immediately as i think of trying to help my 93-yr-old mother asap: 1) Hydergine--doesn't that help rid the amyloid "plaques" and "liver spots"? Also, 2) IV chelation therapy should help this process, especially in blood vessels around the heart if done long and regularly enough?
If there are better practical procedures available NOW, kindly let me know before I talk to Mom's doctor about beginning these two decades-old practices on Mom. (I did them myself in the 80s and 90s--probably a good idea to do them again on myself, too?)
Thanks...
I have just heard about this new drug CPHPC. Is it available for clinical trials? Does it have any side effects? My Mom is 85 and she lives with me. I would love for her to talk to me and atleast respond to simple questions and of course swallow her food ( she has to be coaxed to do so)
Can any body help?? Am i being rash in asking for this drug? Mom does not know me since last 7 years
I just want her to know me.
Thank you
I'm a very fit 69-year-old caucasian male who has been diagnosed with Familial amyloidosis after a very extensive set of tests, etc., at the Mayo Clinic in Arizona. While at the Mayo they were starting to advise me to consider a liver transplant. I'm hoping that a magic bullet is developed which would treat my amyloidosis. How do we contact Prof. Pepys to get into the UK-based trials?
jl
@Dr. Joseph Levy: I'm not very familiar with the UK trial system and how to look into what's presently recruiting; I can only point to my US-focused post on exploring the options when you have a condition where progress is in the works but may not arrive in the clinic soon enough:
https://www.fightaging.org/archives/2004/11/researching-therapies-and-participation-in-trials.php
Contacting specific researchers is pretty easy - use Google, look at department websites, be polite and call their department secretary before pinging them directly, etc. As a general rule they're pretty happy to hear from the interested, polite public - it happens less often than you'd think, and it's a validation when it does.
Hi there, i m suffering from lichen amyloidosis since 9 to 10 yrs , wil this cphpc wil help to treat my condition as well?? When will this medicine release in the market. I am from
India , really looking forward with a hope that some medcine come in future n help patients suffering from amyloidosis and free from such dreadful disease. Plz any information or update on cphpc wil be really helpful.thanking you.
My dad was diagnosed with primary amyloidosis (AL) at age 76. It presented as highly elevated BUN and creatinine levels (triple the maximum limit), which his GP had ignored or passed off as old age. Once diagnosed, he was given melphalan with no benefit, and his bone marrow was clear of cancer. He was then put on hemodialysis, but continued to deteriorate due to the AL (thyroid was badly swollen and 2/3 of it was removed at age 79 so he could swallow and breathe properly). He had bowel disruption, poor nutrition, loss of apetite, weight and strength loss, and finally shortly after turning 80, elected to end dialysis and go into hospice, where he passed away after 19 days.
We contacted Dr. Pepys and pleaded at any expense to allow my dad to participate in trials, but he was not allowed to. My family is very interested in finding a promising released cure, and Dr. Pepys' approach of at least a maintenance drug looks like the best path. We hope that the cause will be found someday. I suspect that chronic exposure to mold from a damp basement and poorly ventilated house was my dad's major risk factor, and would love to hear from others who suspect the same from their relatives.