A Potential Breakthrough in Alzheimer’s Disease

by | Jan 26, 2022

I write this newsletter with a heavy heart – my closest friend and colleague has been diagnosed with dementia and/or Alzheimer’s disease (AD). My friend (now retired) is partially responsible for having created the lifespan assessment tool we use in our life settlement business, so he has an indirect connection to everyone reading this newsletter.

The rise of AD in our modern world is not unexpected, and as you may be aware, I’ve published extensively on the topic of how AD could rise in prevalence dramatically in the coming years because of a phenomenon known as “competing risks”. This is an argument suggesting that as progress is made against one set of diseases, because death is inevitable, a decline in one cause of death must eventually lead to a rise in another.

A cure for cancer or heart disease would be most welcome to be sure, but population health scientists like me tend to look at the big picture and not just the immediate effect of breakthroughs in treating specific diseases. The survivors of such breakthroughs would surely live longer, but one important consequence would be a dramatically accelerated risk of developing AD and other cognitive and physical impairments.

For people now facing the consequences of success in living in these bodies beyond their biological warranty period – which is the case for my friend – until a breakthrough in aging biology comes online, the question is; what can be done now?

There are several ‘treatments’ for AD that are now part of the arsenal of weapons used once patients are diagnosed, and you can learn about them here. Honestly, none of the current ‘treatments’ work particularly well, and the newest approved drug – aducanumab – is controversial, and some scientists in the field believe the side effects could be worse than the condition itself. The language used by researchers in the field on the effectiveness of current treatments is unambiguous– “Unfortunately, none of the pharmacologic treatments available today for AD have yet been shown to inhibit or slow down the damage and neuronal death ultimately leading to morbidity and mortality associated with the disease.” Source, p.2

However, once my friend was diagnosed with this condition, I went to several friends and colleagues in the field who study AD for a living, and they all pointed me to a new AD treatment that is being tested now. In fact, the evidence of potential benefit was so strong that I’m attempting to see if my friend qualifies to enter into the next phase of the clinical trial.

What is interesting about this new treatment is that it’s not a drug – it’s a filter that is used outside of the body (referred to as Plasma Exchange) that essentially removes compounds contained within the bloodstream that are believed to contribute to the rise and progression of AD. For those of you that like to read the key findings in an article, I’m including the language below (source provided above).

Plasma exchange (PE) with albumin replacement is being investigated as a new therapeutic approach for AD on the basis that Aβ in the cerebrospinal fluid (CSF) is in dynamic equilibrium with plasma Aβ through the blood-brain barrier and that sequestration of Aβ in the peripheral blood would alter such balance to induce CSF Aβ to pass to plasma. Hence, routine PE removal of an AD patient’s plasma would favor elimination of albumin-bound Aβ, and possibly, other pathogenic elements. In addition, replacement with fresh therapeutic albumin can restore the antioxidant capacity of AD patient plasma, as albumin is highly oxidized and glycated. Furthermore, a therapeutic action at the vascular level can have a positive impact on dementia.

The treatment was most effective in AD patients with moderate disease (e.g., more advanced) relative to patients diagnosed with mild AD. The sample size was large enough to warrant statistically significant results, and while some adverse effects were observed in a small percentage of the patients under treatment (this is the case with almost all medical and pharmacological interventions), the evidence clearly showed an ability of Plasma Exchange to slow cognitive and functional decline.

While PE is not yet ready for prime time, for patients that are sliding down a pathway toward severe AD, any treatment that slows the process (especially if it does not involve the use of drugs), is deserving of serious consideration.

I don’t know whether my friend will qualify for the next phase of the clinical trial; nor do I know whether he and his family and neurologist would consider this an option; but at least now they’re aware of something new that is in a phase 2b/3 trial. This means the treatment is considered safe, and now researchers are working on a more detailed test of efficacy.

In the interim, researchers in the field of aging are still working on a therapeutic intervention to slow aging itself. While funding for this line of work has risen dramatically in just the last year, it is uncertain whether the treatments being tested will arrive in time to help out my friend and the millions of others across the globe facing a daunting challenge imposed by dementia and AD.