Thoughts on Dementia, Parkinson's and Alzheimer's- Part 2

Thoughts on Dementia, Parkinson's and Alzheimer's- Part 2

A year ago I wrote my first blog on the big three chronic brain disorders that I hope to avoid as I age.  I concluded that adding bioavailable astaxanthin to my diet can help keep my neurons operating at peak efficiency. 

I continue to follow the scientific literature and have found clinics offering  Nicotinamide adenine dinucleotide (NAD) supplementation as a promising therapy for Alzheimer’s disease (AD).

Should I be taking NAD+ supplements as well? 

This blog delves into brain cell energy production, the vital role NAD plays in that process,  and the relationship between NAD and bioavailable astaxanthin.     

( And no,  I am not racing out to get NAD supplements)

Neurons and Energy

Neurons are the most energy demanding cell type in our bodies. 20% of the oxygen we breathe is used to power neurons. To produce that power, neurons are packed an estimated 2 million mitochondria each using glucose and oxygen to provide the power neurons need to function and repair themselves.

Detecting AD

One symptom of AD is a decline in the neuron's ability to generate power (Aka mitochondria dysfunction).   Functional imaging techniques such as positron emission tomography (PET) and magnetic resonance imaging (fMRI) can be used to detect mitochondria dysfunction by looking for surplus glucose inside the neurons.  Scientists including Yang et. al. (1) have linked elevated glucose levels in brain cells with the severity of AD symptoms.

What is NAD+?

Nicotinamide adenine dinucleotide (NAD) is a coenzyme used extensively in every cell of our bodies. 

NAD exists in two forms, NAD+ and NADH.  NAD+ has been depleted of electrons so is positively charged (hence the '+”) whereas NADH is NAD that has gained 2 electrons and a hydrogen (hence NADH). 

NAD and Energy Production

Mitochondria use both forms of NAD, first using NAD+ to make NADH (glycolysis/ Krebs cycle),  then subsequently splitting NADH back into NAD+ using the hydrogen and electrons to make ATP. This chemistry (cellular respiration) has remained unchanged for billions of years.

Reactive Oxygen Species and Energy Production

Under normal conditions,  about 2% of the oxygen that is consumed in the brain is converted by the mitochondria into reactive oxygen species (ROS) which are compounds containing oxygen that have extra electrons. These compounds are highly reactive and can do serious damage if left free in cells.

If we are under sustained stress (too much/not enough glucose, not enough oxygen, too hot, too cold, exposure to toxins etc.) the mitochondria become less efficient at making energy and ROS production increases.

NAD+ Deficiency & Supplementation in AD

Compounds that lose/give up electrons to others are classified as antioxidants.  In this case,  NAD+ has been depleted of electrons and will gladly take them in if available… so it functions as an antioxidant. 

Once this happens, NAD+ has been effectively removed from the mitochondria’s energy making toolkit. The resulting “NAD+ deficiency “ has led to NAD+ supplementation as a potential therapy for AD. 

NAD+ cannot be taken orally as it can't traverse the digestive tract without being oxidized.   Clinics  have popped up offering intravenous (IV) therapies that include NAD+ claiming to restore oxidative balance.  

Astaxanthin & NAD+

Nature created its most powerful antioxidant, astaxanthin,  700 million years ago.

If in the right form and the right place,  astaxanthin will embed itself into the mitochondria plasma membrane and protect NAD+ from being oxidized by ROS. 

Adjuvia Astaxanthin is available in oral form and costs about $400 per year  vs. upwards of $800 for a single NAD+ IV therapy which may temporarily refill the NIH+ gas tank but doesn't repair the leak. 

It’s your brain and your choice. 

1) Evidence for brain glucose dysregulation in Alzheimer’s disease”  Yang An et. al. Alzheimers Dement. 2018 Mar; 14(3): 318–329. Published online 2017 Oct 19. doi: 10.1016/j.jalz.2017.09.011