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By Felix J. Rogers, DO
Over the past century we have seen an interesting comparison between our understanding of coronary heart disease and dementia.
In 1913, in St. Petersburg, Russia, Nickolai Anichkov demonstrated that fatal heart attacks were caused by cholesterol build-up in the blood vessels that feed the heart. Because of the western diet and intense marketing by the tobacco industry, it wasn’t long before heart attacks became the number one cause of death in the US. The Framingham Study, which started in 1948, defined the features of coronary heart disease and effective treatment soon emerged. The incidence of heart disease has fallen steadily since 1968.
Now, contrast that success story to our experience with dementia. In a similar timeframe, Alois Alzheimer described the case of Auguste Deter to the Southwest German Medical Society in 1906. She had symptoms of paranoia, delusions and memory loss for 4 years before her death at age 55. Dementia was felt to be a rare condition and it wasn’t until the mid 1970s that the disease was felt to be the cause of dementia in the elderly. There is no effective treatment for it. The number of patients is rising, especially with the aging of our society. It is now the fifth most common cause of death in the US.
Alzheimer described clumps of protein (amyloid) in the brain of his first patient along with damaged nerve cells and hardening of the arteries. Although amyloid is highly toxic to brain cells and was presumed to cause the disease, not a single research trial with amyloid as a target for treatment has had any significant value.
Even though effective treatment of Alzheimer disease (AD) continues to elude us, a new understanding of the pathology of the disease provides encouraging news for its prevention. Researchers have now shifted their attention from the amyloid protein to the blood vessels of the brain (and the rest of the body, for that matter). They were prompted by the paradox that a high number of people who were felt to be normal before they died will have autopsy findings consistent with Alzheimer disease and conversely a significant number of people have almost no evidence of amyloid plaque at autopsy but were severely demented. Something else is going on.
That something else has been traced to cholesterol build up and to abnormal function of the blood vessels. We now know that abnormalities of the vasculature are common in patients with AD. These abnormal vessels are found throughout the brain and explain many of the manifestations of dementia. Because the function of these vessels is abnormal, they allow a disruption in the blood brain barrier that is essential to protect our brain from inflammation that occurs as a result of infection, systemic toxins and the metabolic abnormalities that can occur with diabetes, hypertension, high cholesterol and cigarette smoking. Furthermore, disturbances in the very small vessels are a double whammy: the disruption in the blood brain barrier and resultant inflammation leads to increased amyloid production and the decrease in blood flow is associated with decreased amyloid clearance.
These findings have led to the discovery that the risk factors that contribute to dementia in many ways are identical to the risk factors for heart disease. The World Health Organization tabulated those risk factors in a comprehensive report in 2019. The Harvard Health Blog then summarized the recommendations for prevention of dementia:
Although many patients are worried that taking statins can cause dementia, recent comprehensive, scientifically controlled studies show that they are safe, and in certain subsets of patients will actually reduce the risk of cognitive decline. Other non-cardiac factors associated with reduced risk include higher educational and occupational attainment.
Felix J. Rogers, DO
Felix is a cardiologist in the Henry Ford Health System and author of The Maggie Letters, a medical memoir that tells how he drew on resources of the family, science and the spiritual journey to cope with his mother’s Alzheimer disease.