In 1906, Dr. Alois Alzheimer performed a brain autopsy on one of his recently deceased patients, Auguste Deter (55 years old), who had suffered for years with a rapid decline in memory, an inability to care for herself, and recurrent delusions. During that autopsy, Dr. Alzheimer identified changes within the brain that he attributed to her disease, making Auguste Deter the first person to be diagnosed with Alzheimer’s disease.
Though this diagnosis has been hotly contested over the years, it is clear that Auguste Deter had some deteriorating condition that dramatically affected her cognitive function at such a young age. What many don’t realize is that the condition that Deter had, defined as Alzheimer’s disease, and the Alzheimer’s disease we commonly see may actually be two entirely different conditions.
Early-Onset Alzheimer’s Disease: The Original Alzheimer’s Disease
Early-onset Alzheimer’s disease is defined by having noticeable and measurable cognitive decline and other dementia-related symptoms before the age of 65 years old. This is likely what Auguste Deter had, making her the defining patient for this disease.
Fortunately, this is an extremely rare condition, affecting 24.2 per 100,000 Americans aged 30–64 (0.024% of the U.S. population aged 30–64). It is thought that this form of Alzheimer’s disease is largely driven by genetics, a few of which we can accurately measure — PSEN1, PSEN2, and APP.
If you have a known family history of dementia in relatives before the age of 65, you should take extra precautions with your brain and have regular monitoring by physicians skilled in this area.
Though early-onset Alzheimer’s disease can present with memory loss, it also tends to come with increased deficits in visual and language processing, such as an inability to recognize faces, visuospatial deficits, and an inability to remember common words in conversation. This makes it much more difficult to recognize and diagnose, as many other conditions can contribute to similar deficits.
Late-Onset Alzheimer’s Disease: Is It Something Else?
Late-onset Alzheimer’s disease is the far more common form of Alzheimer’s disease, affecting more than 7.4 million Americans over the age of 65. It is defined by a relatively slow loss of cognitive function and inability to care for oneself independently.
But is this the same thing as the early-onset variant?
We have historically grouped early- and late-onset disease together largely because they share similar pathology. But sharing pathology does not necessarily mean sharing the same pathogenesis.
Increasingly, researchers recognize that late-life cognitive decline is remarkably mixed, with Alzheimer’s pathology interacting with vascular disease, metabolic health, inflammation, and genetics. It behaves differently, its risk factors are entirely different, and it’s likely the reason that we are no closer to finding a drug treatment despite having an annual budget of $3.9 billion.
Looking back on the WHO Guidelines and Lancet Report on dementia prevention, you can see that we are able to reduce dementia risk through a wide variety of pathways:
- Nutrition
- Exercise
- Sleep
- Social connection
- Learning
- Avoiding traumatic brain injuries and strokes
- Addressing vision and hearing loss
- Avoiding insulin resistance, pre-diabetes, and type 2 diabetes
- Reducing blood pressure
- Treating obstructive sleep apnea
- Reducing cholesterol levels
- Menopause hormone therapy?
- Ensuring proper nutrient availability (omega-3s, B vitamins, etc.)?
- Understanding your ApoE status
The only other disease state I can think of that behaves similarly would be cardiovascular disease. We know multiple pathways that contribute to vascular disease, and intervening early is far more successful than treating disease once it has happened.
Nobody wants to wait until they have a heart attack to care about their heart. So why should we think any differently about our brains?
What Even Is Alzheimer’s Disease?
Many will state that Alzheimer’s disease is due to the collection of abnormal proteins in the brain called amyloid and tau. And it is true, people with Alzheimer’s do have elevated levels of these proteins in their brains.
But we can also point to patients with perfectly normal cognition who also have high levels of amyloid and tau on brain scans.
We’ve spent billions of dollars on treating amyloid, using powerful drugs that literally dissolve amyloid from the brain. But the results have been fairly lackluster. Marginal benefit if early in the disease course, and little to no benefit in more severe cases.
Though amyloid and tau are hallmarks in Alzheimer’s disease biology, they are not sufficient for the diagnosis.
Dr. Richard Isaacson, one of the leading preventative neurologists (also my favorite neurologist!), recently stated that he had no clue what Alzheimer’s disease (i.e. late-onset) actually is. Rather, he believes that late-onset Alzheimer’s is simply an end-stage presentation of neurodegeneration as a result of numerous insults to the brain over decades.
It is not a singular entity, with a protein you can detect and treat. It is not a genetic process you can just turn off. It is what happens to the brain that is damaged over time.
I think of this as similar to death. Death is not a disease in the sense that we can diagnose and treat it. We may be able to slow down our progression toward death, but it is an inevitable reality of our life.
Natural death is, in a way, the final result of decades of wear and tear and destruction of our body’s major organs.
For Late-Life Dementia, Prevention Is Treatment
We will never be able to treat death with a pill, just like I don’t believe we will ever be able to treat late-onset dementia with a pill.
To truly “treat” dementia, we need to take a zoomed-out approach, caring for our brains over our entire lifetime. We need to think early and often about the strategies we can take to slow down brain aging, to avoid brain trauma, and to increase our brain resiliency and power.
We need to think of prevention as treatment, rather than waiting for a magical drug to come.
The field of dementia prevention is growing rapidly, and I believe we are on the cusp of incredible insights into how we can best address late-onset dementia before it even starts.
No matter how old you are or what level of cognition you have, you can always start somewhere.
Get interested in your brain, and let’s start caring for it together.
At Authentic Health in Asheville, NC, we believe that understanding your health means looking at the bigger picture — including the factors that influence brain health and healthy aging over the course of a lifetime.