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Reason Found Why So Many Promising Alzheimer’s Treatments Eventually Fail

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Reason Found Why So Many Promising Alzheimer’s Treatments Eventually Fail

Reason Found Why So Many Promising Alzheimer’s Treatments Eventually Fail
October 01
19:35 2018

Over the past year, I’ve written about a number of new tests that show promise for treating Alzheimer’s disease. Millions of dollars and tens of thousands of man hours are being spent all over the globe studying what causes Alzheimer’s and how to slow it down or even reverse the damage.

The conventional or prevailing theory is that over time, beta-amyloid proteins build up in the brain and that once they accumulate enough, they begin to kill of brain cells. Additionally, tau proteins also build up and disrupt the signaling between nerve cells in the brain. The combination of the build up of the two abnormal proteins results in Alzheimer’s, a deadly form of dementia.

Some recent research, while admitting that beta-amyloid and tau proteins play a role in Alzheimer’s, questions the exact effect of these proteins and if there may be more to Alzheimer’s than what the prevailing model explains. It’s also believed that another protein, Dickkopf-1 (Dkk1) also has a role in causing the damaging of nerves in the brain.

This questioning has come from the fact that so many of the different research studies that look so promising in the treatment of Alzheimer’s eventually fail to meet the early trial results. So many of them look so good at the onset, but then for reasons that have been bewildering to researchers, the promising results soon fade away and they end back at square one. This is why you read the many posts about a promising treatment but then you hear no more about that experimental treatment.

Richard Killick, the senior author of study from King’s College in London, explains why so many promising treatments end up failing:

“We show that a vicious positive feedback loop exists in which beta-amyloid drives its own production.”

“We think that once this feedback loop gets out of control, it is too late for drugs which target beta-amyloid to be effective, and this could explain why so many Alzheimer’s drug trials have failed.”

What Killick found was that as beta-amyloid begins to build up on nerve cells in the brain, the cells begin to retract their extensions at the synapses with other nerve cells. This retraction in turn causes the production of more beta-amyloid and thus the vicious loop begins.

Most promising treatments fail because they don’t address this vicious loop, so while they first show promise, the loop continues and defeats the new treatment.

What Killick and his team are looking at is a way to break the feedback loop and he thinks they may have possibly found something to help:

“Our work has shown that we may already be in a position to block the feedback loop with a drug called fasudil which is already used in Japan and China for stroke.”

“We have convincingly shown that fasudil can protect synapses and memory in animal models of Alzheimer’s, and at the same time reduces the amount of beta-amyloid in the brain.”

Don’t get too excited yet. There needs to be more research to see if in fact fasudil does what they think it does. It will take time to determine if it helps or not. At least the bright part of this research is that they have learned why so many others have failed.


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