When did the medical world’s continuing journey toward understanding what causes Alzheimer’s disease begin?
In 1901, overcome with grief following his wife’s death, Alois Alzheimer poured himself into his work at the “Castle of the Insane” in Frankfurt, Germany.
Then on November 26, 1901, the neuroanatomist and clinical psychiatrist conducted a clinical investigation of a newly admitted patient, Auguste D. At age 51, she was experiencing:
- sleep disturbances
- memory disturbances
Her symptoms continued until she died in April 1906, when Alzheimer examined her brain and found “plaques” and “tangles.” In November of that year, he shared his case study at a symposium of German psychiatrists.
When he told of his findings, they didn’t generate much interest.
However, Alzheimer’s psychiatric associate Emil Kraepelin found the discovery sufficiently fascinating to include “Alzheimer’s disease” in the 1910 edition of his Handbook of Psychiatry.
And in his memoir, Kraepelin wrote, “Alzheimer, a neuropathologist, has found these very specific changes in the brain of his patients. It’s plaques and tangles. We all know that dementia is primarily a matter of arteriosclerosis.”
Albert Hofman, M.D., Ph.D., delivered this paraphrased Kraepelin quote in a 2019 lecture posted on Harvard University’s YouTube channel.
As chair of the Department of Epidemiology at Harvard T.H. Chan School of Public Health and a founder of the Alzheimer’s Cohorts Consortium, he’s one of the world’s leading authorities on Alzheimer’s disease.
Over 110 years have passed since Emil Kraepelin recorded his thoughts on what causes Alzheimer’s disease. From what we know today, was he correct about the Alzheimer’s arteriosclerosis connection?
Conflicting Answers To What Causes Alzheimer’s Disease
A common belief is that aging is what causes Alzheimer’s. However, Dr. Hofman strongly suggests that an accumulation of risk factors, and not aging, is responsible.
Another belief about what causes Alzheimer’s disease is that it’s inherited. Some parents pass down genes that make their children more susceptible to developing the condition.
And in the 1990s, research first associated three significant genes with Alzheimer’s:
- Presenilin 1 (chromosome 14)
- Presenilin 2 (chromosome 1)
- APP (chromosome 21)
However, Dr. Hofman points out that these genes represented less than 1 in 1,000 cases (or 1/10 of a percent.)
Nevertheless, genetics studies since then have identified additional genes linked to increased Alzheimer’s occurrences.
They include an association with Apolipoprotein E (APOE), which occurs only in people who inherited a “double dose” of APOE. They, too, are a tiny percentage of the population.
And APOE also helps regulate fat metabolism. So it may have a similar link to vascular changes.
The third gene with associations to Alzheimer’s is the microtubule-associated protein tau (MAPT). Again, this gene doesn’t seem to represent a large part of the population.
Other common answers to the question of what causes Alzheimer’s include:
and atherosclerosis-related disruptions in blood flow to the brain.
Dr. Hofman’s Expert Ideas
Despite so many speculative causes, Dr. Hofman seems to agree with Emil Kraepelin’s original hypothesis:
Alzheimer’s disease is largely a consequence of atherosclerosis.
One of his studies found that people with more advanced atherosclerosis had higher rates of Alzheimer’s. Those with double the arterial plaque experienced three times the rate of dementia.
Some people think anything less than 80- to 90-percent arterial blockage isn’t a cause for concern.
But Dr. Hofman suggests that blockages less than 50 percent still result in “chronic hypoperfusion,” or insufficient blood flow to the brain.
A small amount of atherosclerosis lessening blood flow to the brain may not appear to do much short-term damage. But over 20, 30, or 40 years, it could impair brain function.
Even more alarmingly, blockages of the small blood vessels within the brain can lead to “silent strokes” fatal to brain tissue.
These small strokes (also known as silent brain infarcts or SBIs) result in a 200- to 300-percent higher risk of a severe stroke, dementia, and depression. All are linked to Alzheimer’s.
How common are SBIs? Some estimates say they affect approximately one-third of people over 70. To stop them, we must beat atherosclerosis.
And thanks to Dr. Kraepelin’s and Dr. Hofman’s answer to what causes Alzheimer’s disease, we realize that the condition is often preventable.
One of the easiest ways to prevent it is to choose a healthy diet. Dr. Hofman suggests that nutrition plays a more significant role than genetics in determining who gets Alzheimer’s!
What type of diet does he recommend we avoid? In his words:
“…[A]ll dietary patterns that are related, particularly to cardiovascular disease or vascular factors, are most likely involved… directly or indirectly, in dementia and Alzheimer’s disease as well.”
This much, we know:
- Dietary cholesterol consumption is connected to cardiovascular disease.
- Just one diet is completely devoid of cholesterol: A plant-based one.
So for heart AND brain health, a plant-based diet is the best logical choice!