Alzheimer: Your diet may contribute to the development of Alzheimer’s disease (AD) in the future. That’s because a new study indicates that a protein produced in the liver in high-fat diets can cause vascular inflammation in the brain, neuron degeneration, and organ atrophy.
John Mamo of Curtin University in Bentley (Australia) led the study published September 14 in the open access scientific journal PLOS Biology. According to the results, amyloid protein (A-beta) produced in the liver can cause neurodegeneration in the brain and play an important role in both the onset and progression of AD.
Previous research has already found that the occurrence of Alzheimer’s – a disease that causes dementia, memory loss and cognitive difficulties, usually at older ages – is linked to the beta-amyloid protein. It clumps in the brain, forming plaques that help in the degeneration of its functions.
The new study indicates that the beta-amyloid protein naturally present in peripheral organs (A-beta) has blood levels correlated with its load in the brain. When in excess, it causes cognitive decline—which increases the possibility that peripherally produced A-beta contributes to the disease.
The problem is that the brain also produces A-beta, which makes it difficult to know where the protein is coming from: whether the main organ of the nervous system or other peripheral organs. As researchers reported in the study, it’s a challenge to distinguish each of the sources.
To perform differentiation, they created a mouse capable of producing human A-beta protein only in liver cells. The protein was carried in the animal’s blood by lipoproteins rich in triglycerides – just as it occurs in humans – until it reaches the brain.
The findings were surprising: Scientists found that the protein caused mice to develop neurodegeneration and brain atrophy, accompanied by neurovascular inflammation and dysfunction of brain capillaries—both commonly seen in Alzheimer’s disease. The affected mice also performed poorly on a learning test that relies on the function of the hippocampus, a brain structure that is essential for the formation of new memories.
The study results indicate that A-beta generated outside the brain is indeed capable of causing neurodegeneration — suggesting that A-beta produced in the liver is a potential contributor to the development of AD in humans. It remains to be seen how much.
If the contribution of liver protein to the onset or progression is significant, the discovery may help in the understanding of Alzheimer’s disease, a search that has focused efforts on the overproduction of A-beta in the brain, and in the vast majority of AD cases, production is not considered central to the development of the disease.
The approach to the disease may change, as the new study indicates that factors such as lifestyle may play a more important role than protein production in the brain. If the theory is confirmed, lipoprotein-lowering drugs may also be developed in the future. Soon, more studies should be carried out to confirm the role that liver protein plays in the development and progression of the disease.