It’s not just in media, high tech and politics where hype often overwhelms hope. It also happens in medicine. The discovery of abnormalities in amyloid and tau proteins made researchers in the 1980s believe they had a handle on Alzheimer’s disease. A host of medications promised to stall or push back its manifestations.
The benefits were oversold.
Today, another “new era” is dawning. New combinations of scanning and brain imaging will define a precise “pre-Alzheimer’s” state. The drugs of old will be used “earlier,” to show they will prove more effective. By catching the disease before it’s fully formed, dementia will be prevented.
The problem with this scenario is that it is too clear, too simple, and too flavored by those betting big money on their imaging/diagnostic/treatment regimens. The truth is that Alzheimer’s, like cancer, is more complicated than it looked – or looks. And much can be done now to prevent disease in the future – without the aid of as yet unproven technologies.
How Do We Know?
Long ago the Okinawa Project looked at centenarians – people who lasted to a hundred and more years. At the time of death, autopsies were performed – particularly of the brain.
Loads of Okinawan centenarian brains appeared to have “horrible” Alzheimer’s. The neurons were filled with Alzheimer’s plaques and neurofibrillary tangles.
Except the decedents did not clinically demonstrate the disease.
How do you get pathology without the disease?
Some of the researchers at the Okinawa Project thought they had the answer – clean arteries. Many of those with “horrible” pathology but reasonable memory had remarkably unatherosclerotic arteries.
And that fit with other evidence. Alzheimer’s is more common in diabetics. It’s more common in people with heart disease and stroke. It’s more common in people with high blood pressure.
Just as cancer appears to be a “multi-hit” kind of phenomenon – with many changes together leading to disease – Alzheimer’s looks the same way. Much of the time you may need to have clogged arteries to make the disease clinically severe.
Sadly, most populations, especially in the West, start developing diseased arteries in childhood and adolescence. Plus there’s much more to Alzheimer’s than neurofibrillary tangles, amyloid and tau proteins.
The Rest of REST
Recently a group under Dr. Bruce Yankner at Harvard has discovered something most curious – the appearance of infantile proteins in elderly adults.
The same major protein also disappears in people with cognitive impairment.
The protein is known as REST. It first shows up infancy, during the development of the nervous system.
It reappears in periods of stress. One thing it seems to promote is decreased nerve cell death. That may be fundamentally important for elderly nerve cells that do not regenerate as well as young ones.
So REST levels fly up among elderly folk. However, they really drop when people develop Alzheimer’s.
Is this an epiphenomenon? Are you seeing less of a regenerative protein because of Alzheimer’s, or is the loss of the protein – and the many systems behind that loss – provoking the development of dementia?
In the next few years we might know. But the Alzheimer’s situation is more complicated than many researchers – and pharmaceutical companies – have told the public.
Lots of other interesting results about Alzheimer’s have appeared of late. One research group went on a targeted “fishing expedition.” They looked at different lipid levels in older folks, then followed them up.
A group of about ten different lipids, or fats, was pretty predictive of who ended up with mild cognitive impairment – and Alzheimer’s.
Will this result hold up? Such studies are expensive. Now they will probably get done. The results make biological “sense” – most of the lipids identified are involved in inflammation.
Again,whether they are cause, result, or epiphenomenon is not known. But combining a variety of potentially predictive technologies, from gene expression changes to lipid levels to imaging results, should help define the prognosis of the disease.
That’s still leaves us a long way from treating it.
What To Do Now
Alzheimer’s is a giant scourge. It’s already killing many millions. As humans live longer, it will kill many millions more.
Research will advance – as it has with cancer. The multiple systems involved with Alzheimer’s – from blood vessels to nerve cells to the glymphatic system – the huge interstitial fluid shifting program controlled by glia cells – will find their place in the bigger picture.
But just as with most regenerative information systems, the answers will probably not prove simple. Which means treatment may not prove simple, either.
Instead, prevention is called for. And many of the major culprits that increase Alzheimer’s risk are the same ones that increase all kinds of mortality. They are risks like high blood pressure, diabetes, obesity, social isolation.
People need help now.
So while research continues, you need to do things that work. Like getting people to walk. Letting them take aspirin and other anti-inflammatories to prevent inflammation of many types, though this has not always been directly linked to decreasing Alzheimer’s. Getting them to eat less processed foods; pushing them out and about, as people who move around and visit others have less heart disease – and Alzheimer’s.
The same stuff that helps people regenerate and grow new brain cells – like walking in nature – will also help prevent dementia. Dementia, rightly, scares many people. But there are strategies that work to prevent it.
We need to use them now.
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