Dementia Related Post

Next are Human Trials…

Only 6 minutes long…. Click Play Button above…

In an earlier piece, I discussed this new drug for treating those with Alzheimer’s by safely removing Amyloid Plaques from the brain.

The drug is Aducanumab.

The link below takes you to that article. It’s only 5 minutes long, so a quick listen.

I’ve been researching a bit more about Aducanumab. There are so few optimistic hopes when looking at treatment for any Dementia that I thought this might be a possible consideration.

My research is mainly around the work of Professor Takashi Asada, of the Emerilas University of Tsukuta, Japan and a leading authority on Dementia.

I’ll first explain how the Amyloid Plaques develop and then how they are looking to remove them.

When brain cells are active, they produce waste. This waste is called Amyloid Beta. The waste is usually broken down by the bodies natural enzymes. However, as we age, this enzyme weakens, and more of the waste, the Amyloid Beta, remains within the brain.

This growing number of untreated waste starts to clump together, forming what is known as Amyloid Plaques. These Amyloid Plaques begin to interfere with the neurones ability to transmit a message from one to another, and eventually, they die. Amyloid Plaques are also referred to as Senile Plaques.

Since the term Alzheimer’s was first used in 1909, the greatest amount of research has been to the pursuit of understanding Amyloid Plaques and their removal.

In 1999, Doctor Dale Shenk, was researching this subject in America. He found that if Amyloid Beta was injected into mice, the bodies immune system started to attack and destroy the Amyloid Beta. This discovery led to significant interest around the World, and in 2000 human trials began.

Two hundred eighty people with Alzheimer’s took part. A Th1 immune cell became active and started to attack the Amyloid Beta as expected.

However, the research came to a dramatic halt when fifteen of those taking part developed encephalitis, brain inflammation.

It appeared that the Th1 immune cell acted indiscriminately and started attacking living brain cells too.

The trial was cancelled! I could not find out any other information following this time relating to this research.

Professor Asada took this research and forwarded it through his knowledge of the gut’s relationship to the immune system.

70% of our immune system is in the gut.

Rather than injecting directly into the blood system, Amyloid Beta was administered orally. However, this method does not trigger any immune response. To do this, he had to put the gene of the Amyloid Beta, which is in all humans, into a Viral Vector. A Viral Vector is a simple virus shell without the virus, like an eggshell without the egg.

This is the same method used to deliver vaccines for COVID.

As the body reacts to this gene carrying virus shell, Amyloid Beta is produced. A Th2 immune cell becomes active inside the gut and instructs other immune cells to produce antibodies that attach to the Amyloid Beta rather than attack it.

The antibodies are then released into the bloodstream and are carried around the whole body, including the brain. On finding Amyloid Beta, the antibodies attach as expected.

From this point on, it becomes a bit unclear. It seems that this amyloid-beta, with the attached antibodies, are eaten. I think this may be the brains Glia cells. These are the brain maintenance cells, but I am unsure, so if anyone can clarify this point, I would be grateful.?

The trials were continued and escalated. Ageing monkeys with amyloid plaques were treated. Four months after treatment, they were almost clear of the Amyloid Plaques with no cases of brain inflammation, encephalitis.

Human trials are the next stage, and the World waits with bated breath!

For this research, Professor Takashi Asada MD was awarded, The Journal of Alzheimer’s Disease, Alzheimer’s Award 2005.

Professor Takashi Asada believes in this treatment, and when asked when it should be given, he said that it should be given as a preventative measure around the age of 50.

There are, of course, questions still. I want to know more about that original enzyme we heard of, the one that usually deals with the amyloid-beta waste but becomes weaker with age. Can something be done to support this enzyme?

Also, what happens to the amyloid plaques that have antibodies attached to them? How are they dealt with and removed? Is it via the bloodstream or the brains own cleaning system?

What happens if you do not use this as a preventative measure but start to treat those diagnosed with Alzheimer’s? What happens to them? Do they remain at the mentally cognitive stage that they were treated?

I believe Prevention is the cure and best option. More needs to be done on promoting lifestyle options to help prevent and stave off later Dementia-related problems and many other medical conditions too.

I apologise for using the word lifestyle, but LifeStyle is the buzzword of the day!

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