By Dr. Jim Ferguson

Alzheimer’s Disease (AD) is a cruel condition. It takes away a person’s humanity and then their life. In ancient times a person was considered alive as long as they were breathing. In Genesis 2:7, God “breathed into man and he became a living being.” I imagined this as ensoulment in a previous essay. Later, life was associated with a beating heart and blood was thought of as the life force. Now, we consider the essence of life as residing with our mind.

We lost a giant last week. John Donne once wrote, “No man is an island” and any death lessens us all because we are so interconnected. However, Pat Summitt was special, and we claimed her as one of our own. And when folks die young (Pat was younger than me!) or “before their time” it seems especially poignant.

On hearing of Coach Summitt’s death, my daughter asked me what causes Alzheimer’s Disease (AD). She seemed perplexed to hear there is no cure for this scourge and only limited treatment. With my children, now adults, I sometimes preface my explanations with “It’s complicated.” This is certainly true with AD.

Philosophically, internists are mechanistic people. We want to understand why something occurs. I believe it’s necessary to fundamentally understand how a disease occurs before you move on to what you can do about it. I’ve previously  written about the complex mechanisms operative in Alzheimer’s Disease, but perhaps an update is timely. I apologize in advance for an internist’s view of this all too common disease. Some might compare my explanations to a book on elephants, more than you want to know. But “for inquiring minds,” read on.

Alzheimer’s Disease was first described in the late 1800s by the Italian physician, Dr. Alonso Alzheimer. He described “pre-senile dementia” in a number of patients with early onset senility – as if dementia was understandable if you were old! There are other causes of declining intellectual function, but I’ll focus on this most common type of dementia. The cause of Alzheimer’s Disease remains unknown, and there is no definitive test for the condition other than a brain biopsy. In fact, doctors often label the disease as DAT, dementia of the Alzheimer’s type, when there is no pathological confirmation.

For a long time the culprit in AD was thought to be the accumulation of a protein called amyloid in the brain. It’s unknown whether amyloid accumulates because of an overproduction, decreased clearance or both in some individuals. Researchers can now measure the amyloid burden with special scans. MRIs only show nonspecific brain shrinkage which may, none the less, be consistent with AD. And, even though as amyloid accumulates and cognitive ability declines, many older individuals have amyloid deposits and normal cognitive function. Furthermore, it has been frustrating that research drugs used to combat amyloid deposits have negligible benefits when treating patients with established DAT.

The tau protein also accumulates in AD. This protein is thought to stabilize microtubules along nerve roots. Imagine microtubules as the plumbing of cells which delivers nutrients and removes waste. The tau protein also maintains flexibility and the structure of nerve cells, much like the frame of a house. In AD the tau protein becomes dysfunctional and folds upon itself, producing tangled aggregates and leads to blockage of cellular plumbing and collapse of the cellular frame, analogous to a mine cave in. Furthermore, the dysfunctional tau protein spreads to neighboring nerve cells much like an infection. Research trials are now testing drugs to try and stabilize the tau protein and reverse the damage.

It’s confusing that both the tau protein and amyloid can be seen in normal individuals. Furthermore, both seem to silently accumulate over decades and only years later does the accumulative damage produce recognizable dementia. The latest theory is that the interaction of amyloid and tau proteins produce dementia.

The current treatment of AD, outside of research trials, is cholinesterase inhibitors like Aricept or another agent called Namenda. Like the drugs to lower amyloid burden, available agents have only minimal effects on AD and none of them are curative. The new hope is to use a cocktail of therapies very early in the disease process (if it can be identified!).

Pat Summitt died as a result of AD which was diagnosed in 2011. More important than the cause of her death, Pat Summitt touched us all. I don’t like basketball, especially pro basketball, but I liked the Lady Vols. Pat Summitt, through her tireless advocacy of Title 9, gave opportunities to women athletes and gave us the team sport of women’s basketball. I didn’t personally know the Coach, but I admired her work ethic, her zeal to win and her legendary kindness and toughness. Her players were made into principled, strong women by her leadership and “the stare” that few dared to cross.

Alzheimer’s Disease is a cruel illness that saps our humanity. I read a story recently which imagined a loved one with AD as slowly leaving this reality and being reconstituted elsewhere (heaven). A materialist would find this notion foolish because there’s no proof of heaven. Well, I would counter there’s no proof there isn’t. I can say Pat’s gone from us now, but she remains in our hearts and memories. It is said you’re never “gone” if you are remembered.

I’ll close this arcane eulogy with wisdom from the “The Prophet” by Kahlil Gibran.

For what is it to die, but to stand naked in the wind and melt into the sun?

And what is it to cease breathing, but to free the breath from its restless tides that it may rise and expand and seek God unencumbered?


Only when you drink from the river of silence shall you indeed sing.

And when you have reached the mountain top, then you shall begin to climb.

And when the earth shall claim your limbs,

Then shall you truly dance.


Rest assured, Pat is OK, and is dancing down the court among the stars.