There are a handful of similar changes seen in the neuro-degenerating brain, especially in the case of various forms of dementia, like Alzheimer’s. If we identify these changes and understand the proposed physiological explanation for why they may occur, we can begin to use that knowledge to implement strategies to potentially prevent or halt progression.
First, it should be understood that dementia itself is not a disease, rather a symptom of another disease like Alzheimer’s, Lewy Body dementia, Parkinson’s or Huntington’s disease. It is estimated that over 25 million people worldwide are affected with dementia, with that number expected to balloon to 84 million plus by 2040. Alzheimer’s is the most common and well known, of the age related memory loss diseases.
Probably one of the strongest pathognomonic characteristics of Alzheimer’s is the presence of Amyloid Beta plaques in the brain. A variety of theories exist as to the exact cause behind their origin, and even the nature of their role in the entire process. The accumulation of excess plaques in the brain is a factor that can indeed diminish brain function, but it is not necessarily an underlying cause of Alzheimer’s, rather a destructive result of those underlying causeS.
Some even propose that these plaques may actually serve a protective role against underlying dysfunction, possibly playing an anti-microbial role, with their presence being in response to an infection.
ACTION: Comprehensive analysis including blood, stool & CSF to identify and eliminate possible plaque causing infection. Regardless of if this precise theory is ultimately proven or disproven, addressing any underlying infections is imperative if health on any level, including neurologically, is the goal; making this a highly effective, primary step to take.
Another theory rooted in a potential protective role of these plaques is that they serve as a blockade between a dysfunctional (either over-firing or under-firing) neuron and another neuron it is intending to deliver the message or signal to. Whether the neuron is over-firing and experiencing what is known as excitotoxicity (often seen in seizures) or under firing due to lack of fuel (in the form of oxygen and glucose or ketones), the brain cell is dysfunctional and sending the wrong signal or conveying the wrong message. The plaque deposition at the synapse (where one neuron connects to another; where signal transference occurs) may be the body pulling out all the stops to preserve optimal brain function, and thus attempting to block these aberrant neuronal conversations with a cluster of proteins; the amyloid beta plaque.
ACTION: Start to prevent excitotoxicity by controlling your blood sugar and insulin levels. The brain cells literally can not keep up with repeated heavy boluses of glucose and become damaged, burn out and die because of it. Artificial sweeteners like aspartame, MSG and certain artificial food colorings and dyes also lead to excitotoxicity and should be strictly limited or, in the case of neurodegeneration like Alzheimer’s, outright avoided.
ACTION: Inadequate fuel for the neurons also leads to dysfunction, and eventual brain cell death. When the neuron is deprived of fuel, it attempts to preserve life by lowering it’s energy needs. It does so by pulling back it’s branches or dendrites that connect and communicate with other neurons. This leads to less synapses and diminished brain activity.
It is becoming increasingly acknowledged that the brains ability to utilize glucose (carbs/sugar) as a fuel source diminishes with age. This is seen markedly in Alzheimer’s patients, as well as those with mild cognitive impairment or carriers of the Alzheimer’s risk factor gene, apoe4.
If your brain can’t use glucose for fuel, you best find another source. The good news is there does not appear to be any decrease in the brains ability to utilize ketones for fuel instead. In fact many note enhanced cognitive performance when their brain is presumably running on this by-product of burning fat for fuel, rather than carbohydrates.
Consumption of healthy fats in general needs to be embraced by the neurodegenerative patient. The nervous system yearns for fat, and those with the lowest levels of cholesterol and LDL quite frequently experience increased cognitive decline and mortality in comparison to their fat consuming counterparts. There is a reason that ample studies are continuously being done on ketone boosting MCT oil or actual exogenous ketone esters and salts as a mode of optimizing and preserving brain function for not only Alzheimer’s, but ALS, epilepsy, and many other neurodegenerative conditions.
It was Dr. Mary Newport who back in 2008 noted that by simply adding coconut oil to her Alzheimer’s afflicted husband’s oatmeal, she noted marked improvements in his cognitive function as far as memory, mood and overall function. A ketogenic diet, including MCT oil & coconut oil and some degree of intelligent time restricted eating (aka intermittent fasting) would definitely be the preferable long term strategy, but for those already struggling immediately adding MCT or coconut oil, or even straight exogenous ketones as a stop gap may provide the brain boosting fuel the starving neurons desperately need to maintain or regain function.
So what is an Amyloid Beta plaque anyway? The plaque is a collection of damaged proteins that end up aggregating, or sticking together in a cluster forming a brain blocking plaque. When it comes to these plaques, the riddle to be solved is why are they are forming in the first place. Diminish plaque formation, clean up the existing deposition, and work towards prevention and slowing of progression.
The formation of these plaques and a certain degree of degeneration is unfortunately an inevitable accompaniment to aging and our interactions with this world. The multifaceted approach to amyloid beta plaque prevention and accumulation attenuation rests on a 3 pronged approach:
1) Limit the formation of the plaques to begin with.
We already mentioned above how infections, excitotoxicity, and a reduction in the ability to utilize glucose as a fuel source more than likely contribute to the deposition of our classic Alzheimer’s amyloid beta plaques. So if we start with the practical suggestions above, and work towards limiting exposure to system stressors and toxins that have been shown to damage cerebral proteins, leading to accumulation, clustering, and plaquing, we are well on our way to protecting and preserving the brain.
Inflammation, especially coming from the gut, excess free radicals or ROS (reactive oxygen species) not being balanced by a diet (or if need be, supplements) rich in antioxidants, heavy metals, mycotoxins from mold, trauma (TBIs & concussions), and inadequate sleep (the time when your brain detoxes) can all contribute to the cascade of plaque formation and brain breakdown.
As you can see, this is not a one cause, one solution issue.
Don’t be overwhelmed.
Start to address each of these issues one by one and clear the path for a better quantity and quality of life for you and that brain.
Don’t become a statistic.
Buck the trend.
We got this.
2) Clean up the damaged and misfolded proteins that make up the plaque.
When it comes to proteins, form equals function. The three dimensional folded shape of a protein determines function and can be the difference between help or harm. If proteins are misfolded, they are damaged and start to occupy space, impede function, and aggregate into plaques. There are a few potential ways to encourage the clean up of these damaged proteins, and thus mitigate escalation to the dreaded amyloid beta.
– Insulin & Insulin Degrading Enzyme:
This may arguably be your most important step when it comes to Alzheimer’s. You must get your insulin under control. One of the highest risk factors for developing Alzheimer’s is hyperinsulinemia. This is the cornerstone of Alzheimer’s correlated Type II Diabetes and is problematic for the entire body, but especially the brain.
There exists an enzyme in the body called Insulin Degrading Enzyme (IDE). As the name implies, this enzyme is responsible for breaking down and clearing out insulin. This enzyme has also been shown to play a role in breaking down amyloid beta plaque. If insulin levels are high, the enzyme prioritizes degrading the insulin over breaking down the plaque. Conversely, you lower your insulin levels, we now have more availability and utilization of IDE to break down one of the critical characteristics and perpetuators of Alzheimer’s.
This could very well be the main reason why insulin resistant type II diabetics are 2 to 4 times as likely to develop Alzheimer’s than their non-diabetic counterparts. It is why Alzheimer’s is referred to as type III diabetes or brain diabetes.
Adding more fuel to this fire, people with the Alzheimer’s risk factor associated apoe4 gene have lower levels of IDE. Perhaps one of the main reasons why apoe4 carriers have the increased risk is due to lower levels of an enzyme that breaks down the Alzheimer’s amyloid beta plaque. You couple lower levels of IDE with elevated insulin levels and I’d imagine you have a sure fire bet for a future Alzheimer’s patient or one who declines rapidly.
Apoe4 or not, you MUST address insulin.
If the above described detrimental effects of high insulin or insulin resistance wasn’t enough for you. Let’s wrap it up by adding this. Elevated insulin levels block the body’s ability to endogenously produce ketones. Remember how we noted that the aging brain, and especially the Alzheimer’s brain has a decreased ability to use glucose for fuel, and how this can be circumvented with ketones? Well, internal production of ketones and burning fat for fuel is blocked by elevated insulin levels. Again, attention to and optimization of insulin control is a must.
-Sauna & Heat Shock Proteins:
An increasing volume of research has shown that by exposing the body to a relatively acute stressor, one of the beneficial hormetic outcomes are the production of heat shock proteins (HSP). These HSPs have been shown to repair misfolded proteins, and assist in the degradation, thus preventing aggregation of proteins and the formation of plaques. In addition to the specific sauna use studied (i.e. type, duration, frequency & temperature), HSP can also be generated during exercise & cold plunges as well. Less damaged proteins equals less available material for plaque formation.
-Fasting and Autophagy:
Not only can fasting or time restricted eating contribute to an elevation of the aforementioned alternative brain fuel in the form of fat derived ketones, but it has been observed that after anywhere from 18-36 hours, a process called autophagy takes place. The body literally eats or cleans up damaged tissues, including proteins. Another potential clean up strategy activated through lifestyle modification.
The importance of sleep, when it comes to brain health in particular cannot be overstated. Sleep is essential as the brain literally shrinks and receives a nightly cleansing and detoxifying bath in CSF (Cerebral Spinal Fluid). The more sleep we get, the more potentially hazardous by-products of our daily cortical metabolism can be removed; including damaged proteins. The brain has it’s own lymphatic system called the glymphatic system that is highly active during sleep. Just as the body’s lymphatic system is responsible for removing waste products, damaged tissues and stagnant inflammation, the brain’s glymphatic system does the same.
Sleep is also the time when memories become consolidated.
One more note on sleep: when you are sleep deprived, the adrenal (stress) glands are forced to kick into high gear in order to keep us going. One of the ways they do this is via the release of cortisol. Excess cortisol from lack of sleep, poor diet, or chronic stress has been shown to actually shrink a part of the brain called the hippocampus; an area highly responsible for memory consolidation, and an area commonly atrophied or reduced in size in Alzheimer’s patients.
3) Create Ample Brain Back-Up
A third way to look at the accumulation of these plaques is as a numbers game. The plaques accumulate in the synapses between neurons, squashing communication and thus short circuiting the brain and all it’s function. We would best be suited to hedge our bet against the inevitable neuronal synapse communication disruption, by creating more synapses.
This is referred to as creating cognitive reserve or surplus, and due to the well documented phenomenon known as plasticity (basically adaptability of the brain), we can intentionally engage in activities that will stimulate the formation of more, more, MORE connections. The logic being here, that if we continually increase the quantity of synapses, we can afford to lose a disproportionately smaller amount of synapses; although obviously never the goal.
Fuel for this approach was seen on full display when the brains of 90+ year old nuns (Nun Study of Aging and Alzheimer’s Disease) were imaged. Many of the brains were actually littered with varying degrees of amyloid beta plaques often seen in those afflicted with Alzheimer’s. However, many of these ladies showed no signs of cognitive impairment or decline. This shows that the presence of plaques, even in a high volume, is not necessarily a damning diagnosis. There are various theories as to why the results turned out the way they did ranging from genetic implications (FoxO1, FoxO3a, Nrf2, etc.), to molecular mechanisms involved with caloric restriction (there is that notion of fasting or time restricted eating again).
These ladies lived active lives filled with challenging new activities, learning, social interaction, and enhanced self awareness and spirituality; all activities known to and required to harness plasticity and literally grow more brain cells and more synapses. One could look at the undertaking of these as brief forms of stress to the body as you are stepping out of your comfort zone and demanding the body adapt or plasticize. It is these brief exposures to stressors (like that generated through sensible exercise) that generate a hormetic response capable of creating cellular stress resistance and make the brain cells more resistant to cellular stress and neuronal cell death.
Cognitive reserve. Cognitive surplus. Cognitive back up. Call it what you will, but get some.
Learn a language.
Play an instrument.
Engage in daily physical activity, preferably utilizing the entire body.
Grow and your brain will follow suit.
Lastly, as far as creating back up or surplus, we need to touch on something called Brain Derived Neurotropic Factor (BDNF). This is a chemical that leads to repair of existing brain cells and even the growth of new ones. Piggybacking on our numbers game logic, we obviously want to do all we can maximize the health, function and sheer volume of our neurons or brain cells. Intentionally and habitually engaging in BDNF prompting behavior should be mandatory for all, but especially those experiencing mild cognitive impairment, suspicious or diagnosed with any neurodegenerative disorder including our topic at hand, or even those looking to alter their generic fate despite the presence of one or two apoe4 alleles.
Exercise, particularly strength and higher intensity (don’t be intimidated, it’s all relative) interval training have been shown to be potent stimulators of BDNF.
Not surprisingly fasting and the presence of ketones also appears to boost BDNF. So now we have anti-inflammatory ketones and fasting as drivers of neuro-protective and tropic processes ranging from providing a necessary fuel source, cleaning up damaged proteins, to now actually repairing or growing neurons. A ketogenic diet or intermittent fasting may not be for everyone, but in light of all this, if you or someone you know has a neurodegenerative condition or are concerned about prevention and progression, especially as we age; it seems like a no brainer (bad joke) to at the very least consider it or varying aspects of it.