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The Dirty Little Secret About Cholesterol & Alzheimer's

A University of Cambridge led team of researchers conclude in a new study that cholesterol may play a prominent role in the development of Alzheimer's disease.

Most people have heard of cholesterol, but what exactly is it? 

For starters it’s a waxy substance that can build up inside your arteries, potentially putting you at risk for a variety of health problems. 

It’s now estimated that 71 million people in the United States are walking around with high levels of low-density lipoprotein (LDL) otherwise known as “bad cholesterol.”

Most often, high levels of LDL cholesterol are associated with an increased risk of cardiovascular related conditions like heart disease and stroke, but cholesterol has another important function too. It’s the main constituent of the cell wall.

In a recent study published in the journal Nature Chemistry, researchers suggest that this cholesterol may also be acting as a catalyst for protein clusters called amyloid-beta to form in the brain.1

Researchers have been aware of Amyloid-beta and its contribution to Alzheimer’s disease for years. And when amyloid-beta aggregates, it forms into plaques that destroy brain cells and alter brain function. 

Even so, scientists have had difficulty trying to identify just how the amyloid-beta clusters form to begin with. 

Cholesterol Increases
The Speed Of Aggregation

In the past scientists have been able to ascertain the fact that amyloid-beta molecules don’t typically stick together in the brain due to the relatively low levels of them and the fact that they’re spread throughout the brain. 

The team from Cambridge along with a team from Lund University in Sweden decided to collaborate and investigate how amyloid-beta manages to form into clusters in Alzheimer’s.

They found that amyloid-beta can stick to lipids, an insoluble molecule made up of fats, steroids, phospholipid, and waxes. Of note, was the fact that amyloid-beta was found to stick quite well to lipid cell membranes containing cholesterol.

Once these amyloid-beta molecules are stuck to these cholesterol-containing lipid cell membranes they can then stick to other amyloid-beta molecules that are similarly stuck. 

This is where the cluster formations can begin.

The research team calculated that in the presence of cholesterol amyloid-beta clusters form at a rate 20 times faster than they would without the presence of cholesterol. 

Does Consuming Less Cholesterol
Reduce Your Risk?

In past studies, researchers have discovered a link between cholesterol and Alzheimer’s.

For example, scientists know that certain genes that process cholesterol in the brain have also been associated with Alzheimer’s. But they aren’t sure just how they’re linked.

Even in this recent study, researchers are still unclear as to whether or not dietary cholesterol plays a role in Alzheimer’s. Primarily, because dietary cholesterol does not cross the blood-brain barrier. 

So, while its conventional wisdom to keep the overall levels of dietary cholesterol you consume relatively low, the amount of cholesterol you ingest on a daily basis does not appear to be an issue when it comes to developing Alzheimer’s.

In fact, one of the studies co-authors Prof. Michele Vendruscolo — of the Centre for Misfolding Diseases at the University of Cambridge — says that it’s not the cholesterol itself that is causing the problem. 

"The question for us now," he says, "is not how to eliminate cholesterol from the brain, but about how to control cholesterol's role in Alzheimer's disease through the regulation of its interaction with amyloid-beta. We're not saying that cholesterol is the only trigger for the aggregation process, but it's certainly one of them."

He went on to explain that cholesterol is transported throughout the body by specific “protein carriers” such as ApoE. This gene in it’s mutated form has also been theorized to be a potential risk factor for Alzheimer’s.

As a person ages, these protein carriers become less effective at moving cholesterol around. And future therapeutic endeavors may include drugs that target this process, helping to control the balance of both cholesterol and amyloid-beta in the brain. 

"This work has helped us narrow down a specific question in the field of Alzheimer's research," concludes Prof. Vendruscolo.

"We now need to understand in more detail how the balance of cholesterol is maintained in the brain in order to find ways to inactivate a trigger of amyloid-beta aggregation."

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References:

1. Habchi, Johnny et al. "Cholesterol Catalyses Aβ42 Aggregation Through A Heterogeneous Nucleation Pathway In The Presence Of Lipid Membranes." Nature Chemistry 10.6 (2018): 673-683.

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