What Causes Alzheimer's?
A new theory defines more of what's missing
Posted June 5, 2016
Alzheimer’s Disease scares people, and it should. It is one thing to lose your life – it’s another to lose your mind. Alzheimer’s rates rise with age, and people are living longer. Recent studies show that many Americans now in their fifties will live into their late eighties. Alzheimer’s rates get particularly frightful around age eighty-five. Many who worry that they will not have enough money for retirement have not factored in the cost of potential dementia. What’s the point of being physically healthy if your brain doesn’t work?
Alzheimer’s rates go up when people have diabetes. They increase with high blood pressure. They get worse with depression. Severe sleep apnea is associated with increased Alzheimer’s rates; so do certain lipids in the blood.
Yet to treat a disease, it’s extremely helpful to know what causes it. For over a generation, the standard theoretical model has fingered amyloid/tau proteins as the culprit. And a new theory of how this might happen is just another example of why our emphasis on drugs as the main way to deal with major diseases remains media-tantalizing but foolish.
A New Theory
Recently a group at the Harvard Medical School has come up with a theory for Alzheimer’s that looks both plausible and heuristically useful.
Their argument still builds on the “standard model” that amyloid proteins create Alzheimer’s disease. No matter that in the Okinawa Study, many women with “clear” neuropathological Alzheimer’s disease did not clinically show the disease. No matter that the “hallmarks” of Alzheimer’s disease, Alzheimer’s plaques and neurofibrillary tangles, appear at completely different proportions of patients with age. No matter that proteins like RISC may be important in the creation of Alzheimer’s, but are neglected because they disappear as we get older. For better and often worse, seeing is believing. Amyloid aggregates are there, we can observe them in cases over and over. The human mind appreciates clear narratives. As we witness today in politics and social policy, simple answers are to be preferred to complex ones, even when they’re wrong.
What the Harvard group found was that amyloid protein appears to be part of a “primitive” immune reaction in the brain. Amyloid proteins literally cage bacteria that get into the brain. If they stick around too long, they probably means real trouble.
In elegant work in animals, looking at those with and without amyloid proteins and infectious agents, they make a very good case is made that immunological causes are prominent in Alzheimer’s.
For the brain is special. The blood-brain barrier keeps many chemicals and living beings out of the brain. Plus the brain's own special immune response, with its active fences to keep out “standard” inflammatory responses like white cells, is very different from occurs in the rest of the body. So demonstrating that amyloid is probably part of brain defense mechanisms should point to other inflammatory changes that produce not just Alzheimer's, but other neurological diseases. As the authors note, inflammatory pathways are potential “new drug targets” for Alzheimer’s Disease.
Fortunately for us, there are other ways than drugs to change inflammation.
The Allure of Immortality
Silicon Valley visionaries are very big on immortality. What’s the point of having gazillions of dollars if you can’t enjoy it forever? (Or at least longer than the average guy.) “Individualized medicine” where your genome is mapped and all the potential pitfalls of aging defined in advance promises lifespans of 120-150 years very soon, we’re told.
It's natural for venture capital to venture fantasies, and then get people to buy them.
But the truth is gazillionaires are living longer. According to government statistics, the top 1% of American earners have seen their lifetime expectancy grow three years in last fifteen years.
Three years is how much the overall population would live longer if you abolished all cancer deaths.
But is this increase because of superior medical care? Bigger and better ICUs? New bionic parts?
No. Most of it comes from lifestyle. How people eat. How they move. How they socialize. Their overall level of stress.
The same things that affect Alzheimer’s rates, and heart attack rates, and cancer rates.
In sum, the population’s health is dependent on effort – conscious, directed actions – far more than on drugs and hospitals.
The new Harvard research links this point of view quite directly. The healthier you are overall, the more robust and effective your immune function – both in the brain and outside it. Which means less Alzheimer’s disease.
The information systems engaged in chronic human diseases are remarkably complex. How complicated? The human genome project of the past century is one example. By mapping the human gene, we would discover the “schizophrenia gene,” all the “Alzheimer’s genes,” the answers to why we die.
But nature is not so simple. Instead of a one or a few genes, we discovered hundreds or thousands that might increase risk rates one or three or five percent. Of course, the Human Genome Project mostly looked at the twenty-five thousand odd protein making genes. The millions of control genes in “junk DNA” did not garner such attention.
The Way Ahead
Corporations want profits, entrepreneurs sellable stories. Health is a somewhat different matter. A two pronged approach, involving prevention and treatment is required.
Presently prevention is hardly an afterthought in most American health programs. This is particularly unpleasant for many families who deal with Alzheimer’s, and have experienced just how ineffective the “breakthrough” drugs of the eighties and nineties were - and are.
To improve health requires effort – individual and collective. Until we get a much better understanding of the enormous information layers behind cancer and Alzheimer’s and many chronic diseases, drug companies will promise more than they can deliver.
For the present, prevention is worth a lot more than cure. It's time to fund it that way.