Slow News -- for Now

Of late, I've been struggling a bit to find material that I thing everyone here would find interesting.  I haven't heard of any new breakthroughs in Alzheimer's research, and there's nothing much new with me.  (Good news.). And no new scandals.  (Also good news.)

But this will change.  The first week in March is when the Alzheimer's Association normally releases their annual Facts and Figures Report.  This is always loaded with new insights coming from research, as well as revelations that researchers have been sitting on, waiting for the big moment.  So stand by.

When someone has something substantial to announce, they want to do it when it will get the most exposure.  Important conferences are the best place to do that.  And the most important conference in the world of Alzheimer's research is the Alzheimer's Association International Conference.  This year it will be held in Toronto during July.  So expect interesting things to materialize then.

I have been a little distracted making videos for the Dementia Monster YouTube channel.  Click here.  A lot more effort goes into making a video than a blog post, but my first priority is this blog.  For one thing, there are a lot more subscribers to the blog than the YouTube channel.  (So thank you.)

When I get the Facts and Figures Report, you'll be the first to hear what I find interesting in it.

Social Activity Stalls Dementia -- Really

Tool #2 in the Dementia Toolkit is "Maintain or Increase Social Activity."  But is there a scientific basis for assigning importance to social activity?  Absolutely, and the supporting evidence is getting stronger.

In Beating the Dementia Monster we said that I had met an Alzheimer's researcher, a neurologist with a practice of 22 years, who said that in his experience the most powerful lifestyle factor in brain health is social connection.  When I said I'd heard that physical exercise is most important, he said that people who go to the gym with a friend do much better.

I had a friend named John with dementia.  Our wives were friends, and I didn't meet him until he was already in serious decline.  Eventually he moved into a memory care facility near our home, and I would go visit him pretty much daily.  He was a very pleasant person and easy to talk to ... even when he didn't make much sense.  He said he recognized me each day, but I'm not sure he did.  He  certainly didn't remember my name.

Over the time I visited John, I observed others in the same facility, few of whom had frequent visitors.  My very subjective judgement was that I could observe some of them declining, while John did not seem to decline further.

Until covid.  As soon as covid hit, the whole facility was locked down for a very long time.  Residents ate in their rooms and had no other social activity.  After a few months of this, John died.

I'm not a doctor, and I don't know much about how he was treated for his dementia.  But I am sure that he would have lived a lot longer if his social activity hadn't been cut short.

Which brings me to an interesting study published in the journal Alzheimer's and Dementia, the journal of the Alzheimer's Association.  It was entitled, "Late-life social activity and subsequent risk of dementia and mild cognitive impairment."  The researchers found that maintaining social activity delays the onset of dementia by an average of five, precious years.

Here's another article on the subject.

The research was done at Rush University, where the MIND diet was developed.  They studied 1,923 older adults over a period of seven years, measuring their social activity against changes in cognition.   Social activities they measured included going out for meals, attending sporting events, playing bingo, taking day or overnight trips, visiting relatives and friends, attending religious services, and doing volunteer work.  They controlled for age and physical health.

The researchers noted that 5-year delay in the onset of dementia is worth about $500,000 in health care costs. 

One thing they didn't control for was differences in physical activity.  They said it's possible, for example, that people who visit friends and family often may be more likely to get physical exercise.

So I go down the list of social activities they evaluated.  We don't go to sporting events or play bingo, but we certainly go out for meals (maybe too much?), go on plenty of overnight trips to visit family in Seattle and on the East Coast, attend religious services, and do volunteer work.  I'm an elder in our church, and I've been a volunteer at the food bank for eight years.  And the thing I find most rewarding at the food bank is just working alongside and socializing with other men my age.

So how much of my success is due to the gym versus my social activity?  Or, for that matter diet, fasting, managing stress, practicing Spanish, and sleep?  It's all in the multi-domain approach.  If you're serious, you'll do everything you can.  And it all works.

Get those plaques out early!

I think it's amazing how researchers have shown that you can actually clean the brain of those amyloid plaques we see in Alzheimer's disease.  This has been done with monoclonal antibodies that consume and dispose of the pesky peptides.  But what is the role of the plaques?  Are they a part of the disease process, such that removing them will stop the disease?  Or are they perhaps part of the body's defense against a pathogen causing the disease?  Or are they there for some other reason?

We have discovered that some treatments removing the plaques appear to slow, but certainly not stop the progress of the disease.  Others get rid of the plaques, but the disease continues.  Are there better approaches to removing the plaques that might more reliably improve memory and cognition?

One thought that comes up often is that we need to attack the disease earlier in its progress.  Generally, participants in drug trials are already showing evidence of cognitive impairment.  But, as we discussed in Beating the Dementia Monster, the disease has been in progress for at least 15 years before the first symptoms appear.  And so it's common to read a proposal that we need to start treatments much earlier.  But I haven't seen much success in that area ... until recently.

"Dominantly Inherited Alzheimer's disease" (DIAN) refers to what we called in Beating the Dementia Monster "young onset" Alzheimer's disease.  (We avoid the term "early onset" Alzheimer's disease so as not to confuse it with "early stage" Alzheimer's disease.)  We described the origin of the disease, specifically in the presence of three, relatively rare genes.  These are PSEN1, PSEN2, and APP.  When one of these genes is present in someone's genome, and if it is dominant over its recessive partner, the person carrying the gene is almost certain to develop the disease -- and develop it at a young age.  Usually, this is in the decade of the 50's, but it could even be in the person's 30's.  

This means that, through genetic testing, we can identify people at a very young age -- even from their childhood -- who are very likely to develop the disease .  This is more than that 15 years before those first symptoms.  So, if we can now identify those people, how about starting to administer the treatment at the very beginning of the disease process -- or even before it begins?

That's what they're doing at Washington University, St. Louis.  In a series of three trials, they are trying to stop the disease before it begins or else to interfere with it's progress once it has begun.  The first trial is using the monoclonal antibody "remternetug" to remove the plaques.  They are enrolling participants as young as 18, perhaps 25 years before the expected onset of the disease.  Expectations regarding onset are based on what happened with the participants' parents. 

According to the Washington University web site, "the trial is part of the Knight Family Dominantly Inherited Alzheimer Network-Trials Unit (Knight Family DIAN-TU), a clinical trials platform designed to find medicines to prevent or treat Alzheimer’s disease."  ("TU" signifies "trial unit.")

The researchers hope to enroll 240 participants in the prevention trial, and the participants will receive the antibody treatments for two years.  They plan to start reporting results relatively soon after the first participants complete their two years.  They will be looking for evidence they have obstructed the disease, although it will be way too early to see if the treatment affects memory and cognition.  That will take years of follow up.

So is this it?  Is this how we will establish a pharmaceutical resolution to this terrible disease?  We won't know anytime soon.  If it is effective, and if it's equally effective with other "flavors" of the disease, it will still be a project to determine who will benefit from it.  Certainly the presence of the ApoE4 gene (the one they look for in 23&ME) in someone's genome would indicate this is a promising treatment.  And there are at least 30 other genes that predispose someone to the disease.  So genetic profile will be a starting place.  But don't be holding your breath for any near-term benefit.