Cholesterol may play a key role in the development of Alzheimer’s disease
Scientists at the University of Virginia School of Medicine and their collaborators have found that cholesterol produced by cells called astrocytes is needed to control the production of beta amyloid, a sticky protein that builds up in the brains of Alzheimer’s patients. Protein accumulates in insoluble plaques, and these are a hallmark of the disease. Many efforts have been made on these plaques in the hope that their removal or prevention could treat or prevent Alzheimer’s.
The new findings provide important information about how and why plaques form and may explain why cholesterol-associated genes have been linked to an increased risk of Alzheimer’s. The results also give scientists an important direction for disease prevention.
“This study helps us understand why cholesterol-related genes are so important for the development of Alzheimer’s disease,” said researcher Dr. Heather A. Ferris. Our data indicate the importance of focusing on cholesterol production in astrocytes and transport to neurons as a way to reduce beta amyloid and prevent plaque formation.
Alzheimer’s plaques and cholesterol
While cholesterol is often associated with clogged arteries and heart disease, it plays important roles in a healthy body. The body produces cholesterol naturally, so it can produce hormones and perform other important functions. The new discovery from Ferris and her collaborators adds a new entry to the list of cholesterol responsibilities.
The paper also brings a new perspective on the role of astrocytes in Alzheimer’s disease. Scientists have known that these common brain cells undergo dramatic changes in Alzheimer’s, but have not been sure whether the cells suffer from or contribute to the disease. The new results suggest that they had a contribution.
Scientists have discovered that astrocytes help stimulate the progression of Alzheimer’s by producing and distributing cholesterol to brain cells, called neurons. This accumulation of cholesterol increases the production of beta amyloid and, in turn, fuels the accumulation of plaque.
Normally, cholesterol is kept fairly low in neurons, limiting the accumulation of beta amyloid. But in Alzheimer’s, neurons lose their ability to regulate beta amyloid, resulting in plaque formation.
Blocking the production of cholesterol by astrocytes has “vigorously” decreased the production of beta amyloid in laboratory mice, he reports. It is too early to say whether this could be replicated in humans to prevent plaque formation, but scientists believe further research is likely to provide important information that will help fight Alzheimer’s.
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