My Protocol for Fighting Dementia – What I Do To Keep Brain Health Optimal

My nervous system is the basis of everything I think, do, and feel. To me, it is of utmost priority that it stays in the best possible shape. However, just as any other cell, tissue, an organ, the brain deteriorates over time.

Humans usually peak around 20-25 years in terms of mental capabilities. From then on, it goes downhill for everybody. This includes gradually progressing compromised blood flow, reduced neurogenesis, and lower neuron health. There is no way to prevent this.

Furthermore, as I age, I will progressively and stochastically lose neurons (in addition, to a decline in neuron function), which is likely part of the reason people’s cognitive abilities progressively decline as they age. For the most part, neurons in the CNS are postmitotic cells (i.e., they cannot divide) and neurogenesis is limited to a few select sites.

Even if we could replace neurons, newborn neurons are mostly incapable of replicating the functional connectivity of a dying neuron, particularly the sometimes macroscopic length of the axon. Thus, in contrast to other cells of most organ systems, neurons cannot be replaced. I discuss this in more detail here: Intelligence Enhancement

Dementia 101

While some form of neurodegeneration (e.g., loss of neuron number and function) happens to everyone, not everyone will get diagnosed with dementia.

It is only called “dementia” when neurodegeneration has progressed to the point that mental capabilities become so bad that they severely impair daily living. However, by that point, mental function has usually already been declining for a couple of decades.

“Dementia” is a catch-all term that includes a couple of neurodegenerative diseases that often present in a mix & match form. Most of these diseases are characterized by the aggregation of one or more faulty proteins. For example:

• Alzheimer’s dementia: The brains of people with Alzheimer’s disease are full of extracellular plaques of beta-amyloid and intracellular aggregates of tau protein, though it is still unsure whether these protein aggregates are a cause or a consequence of the disease. There are probably multiple different paths that lead to Alzheimer’s. These include vascular, metabolic, inflammatory, metabolic, toxic, and genetic “versions” of the disease – and it is not even clear whether different “kinds” of Alzheimer’s represent the same “disease”. About 80% of all dementia forms are Alzheimer’s dementia.

• Frontotemporal dementia: Frontotemporal dementia is associated with aggregates of another set of proteins (tau, TDP-43, FUS), particularly in frontal and temporal regions.

• Others: Faulty proteins also accumulate in Lewy body dementia, and Parkinson’s disease (which Parkinson’s is a little different).

While we have identified a handful of clear-cut risk factors, nobody exactly knows why in certain people a certain subset of neurons degenerates. Furthermore, nobody knows whether the protein aggregates are a cause, byproduct, or both.

Tactics I follow to preserve brain health

• Having no ApoE4 allele
• Putting a prime on exercise
• Optimizing metabolic health
• Preventing atherosclerosis
• Optimizing hormones
• Lowering inflammation
• Fish oil
• Preventing nutrient deficiencies
• Rapamycin
• Senolytics
• MAO-B inhibition
• Optimizing sleep
• “Brain stimulation”

The above is only a fraction of the article. This article is currently undergoing final revisions and is expected to be published within the next few weeks to months. To receive a notification upon its release, sign up for my newsletter.