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“I am the CEO of Cellulim and a biologist with a specialization in Ecology, Neurobiology and Aging. Each week I will be breaking down the latest research on Aging and explain how to incorporate Longevity in your Life.”

Is NMN good or bad treating Alzheimer disease, Parkinson disease, Huntington disease and ALS

Posted at July 22, 2022, 12:06 p.m.

Today we are going to talk about neurodegenerative disorder. Neurodegenerative disorder it is a type of disease in which cells of the central nervous system stop working or die. Neurodegenerative disorders usually get worse over time and have no cure. They may be genetic or caused by a tumor, stroke, or the body gets exposed to certain viruses or toxins. Examples of neurodegenerative disorders include Alzheimer disease (AD), Parkinson disease (PD), Huntington disease (HD), and amyotrophic lateral sclerosis (ALS). One of the questions I recently got is, does NMN after injury promotes axon degeneration or does it protects against axon degeneration. Let’s find out.

Let’s start with the central nervous system. The central nervous system (CNS) is the part of the nervous system consisting primarily of the brain and spinal cord. The three broad functions of the central nervous system are to take in sensory information, process information, and send out motor signals.

All this information in central nervous system goes trough neurons. Neurons are the building blocks of the central nervous system. Billions of these nerve cells can be found throughout the body and communicate with one another to produce physical responses and actions.

These neurons are the body's information superhighway. An estimated 86 billion neurons can be found in the brain alone. Most neurons are divided into three basic sections: dendrites, cell body, and axon. And It is the axon of the neuron where often problems occur, one example is axon degeneration? Axon degeneration is a common pathological character of neurodegenerative diseases. It results in the loss of communication between neurons.

This loss of communication between neurons is at the base of all the hundreds of different neurodegenerative disorders, Even-tough many different disorders are known most attention has been given only to a handful, including Alzheimer disease (AD), Parkinson disease (PD), Huntington disease (HD), and amyotrophic lateral sclerosis (ALS).

This los of communication has been discovered for the first time in, 1850 – by Augustus Waller in Londen who noticed that frog nerves degenerate when they are injured. Waller’s observation changed a lot and the process he observed became known as Wallerian degeneration. Which actually means that the neuron only degenerates when it thinks there is damaged to much to function properly. It is important to understand that it is the cell it self who decides to degenerate or not. You can imagine that these findings raise even more questions then answers so unknowingly he started a whole new field later called neuroscience.

More the 100 years later in 1989 - Hugh Perry and Michael Brownin in Oxford, where they routinely where using Waller’s method to make mouse nerves degenerate, which enabled them to study axon degeneration. They did a few test with mice instead of frogs and they discovered that the injured nerves in their apparently normal mice did not degenerate.

At first they where baffled and thought maybe it was a difference between frogs and mice? But that could not be the case because other investigators had already reported ‘normal’ Wallerian degeneration in mice. Perhaps they hadn’t cut the nerves properly? So They repeated the experiment again and again with the same outcome. But when they did the same experiment on an other type of mice they saw the expected degeneration occurring. So they had to conclude that there was something different about these mice.

Could it be that axons also undergo a programmed death mechanism that somehow ‘failed’ in these mice? This opened a whole new research topic. Where they had to find the mechanisms that control this programed cell dead in neurons because you can image that it had huge implication for finding a cure against Alzheimer disease (AD), Parkinson disease (PD), Huntington disease (HD), and amyotrophic lateral sclerosis (ALS).

So the race had started to track down the protective gene. Within 30 years, the first drugs appeared targeting these molecular pathway producing therapies in a range of axonal disorders. This all proved that axon degeneration is controlled by certain mechanisms like specific genes, enzymes and specific molecules.

It not hard to imagine that on day we will be able to cure all early diagnosed Neurodegenerative Diseases. And the question today off this video is, can the NMN molecule play a roll in this endeavor. First NMN is a molecule and a precursor of the molecule NAD+. It happens to be that NAD+ is found in all cells and regulates diverse biological processes, including aging, circadian rhythm and according to the latest research also axon survival. It is well known that NMN/NAD+ does something with axon survival, but the big question here is does NMN increase axon degeneration or does it protect against axon degeneration.

The answer is, it dependents on who you ask. If you ask research group lead by Di Stefano the answer will be, NMN increase axon degeneration and if you would ask research group lead by Milbrandt they will say that NMN will protect from axon degeneration. But how is this possible, these people are well educated and only conclude something if there is hard data to proof it.

The study by Di Stefano demonstrated that a reduction of NMN protected against Wallerian degeneration in vivo in both zebrafish and mice. The method they used is by over expressing an enzyme that converted NMN to NaMN. When they saw the levels off of NMN going down and at the same time recorded reduction of axon degeneration. They concluded that you could protect Wallerian degeneration by lowering NMN.

But the research group lead by Milbrandt showed that boosting NMN levels by over expressing NAMPT actually protects against Wallerian degeneration. The NAMPT is an enzyme that is able to convert nicotinamide to NMN.

Even tough this is very confusing one thing is curtain both conditions created by both research groups also substantially increase NAD+ levels. Which seem to suggest, that high NAD+ levels offset the pro-degenerative effects of NMN.

Ok, recap so we have NMN some researches say it is bad the other says it is good and together they say that the product Nad+ is good.

I am still confused, and If a am confused what about you. Maybe the easiest answer would be more research is needed.

And more research is really needed because preserving axon integrity and function is a viable therapeutic strategy for many neurological disorders. Understanding the mechanism of axon degeneration is, of course, crucial for this endeavor.

Thanks for reading, and start living again because it is over before you even started.

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About Cellulim

After walking trough the ruins of the Mesopotamian civilization our founder realized life is too big to dream small. So he started a company “Cellulim” with a mission to extend human lives in an Alolim economy. After all, life is brimming with possibilities. It’s where “What if” runs away with “Why not?” It’s taking the trail less travels to find a better world. Because deep inside we all feel we can do better, so step up start living again and make this planet a better place to live.

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