Alzheimer’s disease and mitochondrial dysfunction

by Martha M Grout, MD, MD(H)
Medical Director in Arizona Center for Advanced Medicine

Alzheimers’s is not a disease. It’s a complex outcome from the marriage of our genes with our environment, with our lifestyle.

We think of Alzheimer’s disease as a disease of the brain – we jokingly call it “Old Timer’s Disease” and hope that we never get it…

But what if Alzheimer’s disease were really a metabolic disease that happens to manifest primarily in the brain? What if this metabolic disease actually occurs all over the body, not just in the brain? What if we could actually diagnose it YEARS before it became manifest in the brain?

Many of us watched our parents decline into dementia, while their bodies stayed apparently healthy and robust until shortly before they died? We watched their minds slip away, memory by memory, logical thought by logical thought, until the only thing left was their worst fears, and their heartbreakingly healthy bodies.

And we wondered, in our secret hearts, whether this was the path we were also destined to tread … After all, maybe it was in our genes. We were told that the ApoE gene had a lot to do with our risk of developing Alzheimer’s, and the ApoE-4 gene was the very worst one, the one that carried the highest risk. And we were afraid…

And we despaired because we were told time and time again that there is no cure, there is only treatment of symptoms until they get so bad that we are forced into a nursing home, waiting for the grim reaper’s visit.

As recently as 2006 we ready in Nature Magazine: “much power is in the hands of governmental funding agencies and pharmaceutical companies throughout the world that set the budget for Alzheimer disease research. They can maintain the current pace and direction of research, or they can drive new ideas by increasing funding and allowing development of more risky approaches that may be associated with significant reward.”[ii] Nowhere in that issue is there mention of mitochondrial dysfunction or metabolic imbalances. We are still thinking that amyloid beta deposition and neurofibrillatory tangles are the whole story. The final paper in that issue is entitled: Alzheimer disease: progress or profit? How much is it going to cost us to care for these 90-year-old infants?

Sad commentary on the state of medicine, that we can only bemoan our lack of progress, and the lack of drugs to treat the symptoms. We are told over and over that by the year 2050 it is anticipated that we will be spending untold zillions of dollars to treat an elderly population which is relentlessly marching toward dementia.

In 2022 an article published on the Quest Laboratory website states: “In 2021, over 6 million Americans were estimated to have Alzheimer’s disease; this number is projected to increase to 14 million by 2060… The pathogenesis of Alzheimer’s disease has been attributed to neuronal degeneration caused by β-amyloid (Aβ)-containing extracellular plaques and tau-containing neurofibrillary tangles.” End of story. The rest of the article involves description of diagnostic tests and how to make diagnosis early. In the final analysis, the article states: “No pharmacological or non-pharmacological approaches are available to prevent cognitive impairment and dementia due to Alzheimer’s disease.” The article does mention modifiable behaviors – non-specific changes to diet, taking vitamin D, exercising – which “may delay the onset of overt dementia”. Not a very enthusiastic or exciting prospect, or much intimation of successful treatment. The treatment paragraph is called “management” and involves mostly drugs to treat the inevitable agitation, insomnia, restlessness and sometimes aggression that occurs when our minds are so clouded by disease that we revert to our base unfiltered behavior…