Can Reducing Fat Intake Prevent Alzheimers Disease? | Doctor Mike Hansen

Alzheimers Disease is one of the most common forms of dementia. Recently, a study suggested that reducing the amount of fat you eat might help prevent Alzheimers Disease.

Alzheimers Disease is a progressive form of dementia that starts with mild memory loss. As it progresses, communication skills and the ability to manage daily life are lost. Alzheimers affects the areas of the brain that control memory, thought, and language.

Timestamps
00:00 What is Alzheimers Disease?
01:09 Breakthrough Discovery
01:45 The Role of the Blood Brain Barrier
02:09 The Role of Amyloid Beta
02:45 Alzheimers Disease Research (NEW)
04:29 Looking Forward

In 2020, an estimated 5.8 million Americans will be living with the disease. By 2060, this number is expected to triple to 14 million. According to the CDC, symptoms of the Disease develop around age 60. The number of people with Alzheimers doubles every five years after that. By age 85, almost a third of Americans have symptoms consistent with Alzheimers Disease. Scientists have worked hard to understand why Alzheimers develops in some people but not in others. Understanding why and how it develops is the first step to learning how to treat and prevent it. Risk factors for developing Alzheimers include:
• advancing age
• having a genetic predisposition
• having comorbid diseases
• exposure to harmful environmental factors
• making unhealthy lifestyle choices.

Researchers in Australia may have made a breakthrough discovery in understanding how Alzheimers Disease develops. They used mouse models to investigate how amyloid-beta damages the blood-brain barrier. The blood-brain barrier is a multi-layer structure that separates the brain from the bloodstream. It is how the brain protects itself. Researchers found that breaks in the blood-brain barrier caused by potentially toxic fat-protein (amyloid-beta) complexes allowed them to enter the brain, causing inflammation and damage to brain cells. The blood-brain barrier serves as a filter. It controls which molecules can pass from the bloodstream into the brain. It keeps harmful substances and infections from entering the brain while allowing nutrients, oxygen, and water to enter. It also allows cellular waste to pass from the brain into the bloodstream.

Amyloid-beta protein build-up in the brain is thought to cause Alzheimers Disease. Long before any symptoms of Alzheimers develop, microscopic amyloid plaques build up in the brain. Sometime later, tangles of the tau protein develop. Over decades, these plaques and tangles accumulate. In some people, they interfere with normal electrical conduction in the brain.

Though everyone has amyloid plaques, a genetic predisposition and exposure to environmental factors determine whether Alzheimers Disease ultimately develops. Researchers from Curtin University in Australia published a study in PLOS biology. The study showed that amyloid-beta was produced by the liver and combined with fats in the bloodstream. These protein-fat complexes traveled to the brain and damaged capillaries that make up part of the blood-brain barrier.

The level of beta-amyloid in the blood has been correlated to the severity of Alzheimers symptoms. Blood tests are used to support a diagnosis of early-onset Alzheimers. Yet, it has been challenging to distinguish amyloid produced in the brain from elsewhere in the body.

Researchers used mouse models to compare a control group of mice to genetically engineered ones to produce human beta-amyloid in their liver cells. The mice underwent cognitive testing. Those in the experimental group showed signs of cognitive decline earlier than those in the control group. Dr. John Mamo, director of the Curtin Health Innovation Research Institute in Perth, Australia, led the study. Over 90% of beta-amyloid in the bloodstream is transported from the liver to the brain by fats called lipoproteins. Researchers examined samples from both the mice brains and livers. The mice brains showed brain cell degeneration, loss of cells, inflammation, and damage to capillaries. Markers that tracked nerve cell degeneration were twice as high in the experimental group compared to the control group. Further research is needed. It is essential to remember that this artificial model may have supported the hypothesis researchers were evaluating.

Understanding how amyloid-beta gets into the brain opens the door for new potential treatment options. Researchers can explore opportunities to manage beta-amyloid levels in the blood. They might also investigate how to keep beta-amyloid from damaging the blood-brain barrier.
This research is exciting because it suggests that managing lifestyle factors such as fat in our diets can affect our risk of developing Alzheimers.

Doctor Mike Hansen, MD
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