Study: Harmful protein that causes Alzheimer's disease may be produced in liver
Sept. 14 (UPI) -- A fatty protein made in the liver causes the breakdown of brain cells, leading to the development of Alzheimer's disease and other forms of dementia, according to a study with mice published Tuesday by PLOS Biology.
The protein, called amyloid, has previously been linked with Alzheimer's disease, the most common form of dementia, the researchers said.
Deposits of a form of the protein, amyloid-beta, are known to disrupt brain cell function in people with Alzheimer's disease.
However, at least until now, it had been unclear whether the protein, which is produced by multiple organs in the body, was created in the brain or elsewhere.
These new findings suggest the liver may play an important role in the onset or progression of Alzheimer's, the researchers said.
"To prevent and treat Alzheimer's, we need to understand what actually causes the disease," study co-author John Mamo told UPI in an email.
"This study shows that exaggerated abundance in blood of potentially toxic fat-protein can damage microscopic brain blood vessels called capillaries, and leak into the brain, causing inflammation and brain cell death," said Mamo, a professor of health sciences at Curtin University in Perth, Australia.
About 6 million people in the United States have been diagnosed with Alzheimer's, the Alzheimer's Association estimates, making it the most common form of dementia.
The recognition of amyloid-beta deposits in the brains of people with Alzheimer's disease using magnetic resonance imaging, or MRI, has helped make diagnosis of the disease easier, potentially allowing for earlier treatment.
However, no cure for Alzheimer's exists, with available drug therapies only able to slow its progression in some cases.
Understanding how these amyloid deposits develop in the brain could help researchers identify drugs that can prevent them, Mamo said.
In addition, dietary modifications such as lowering consumption of high-fat foods, could "potentially" slow production of these proteins in the liver, thus reducing blood levels and preventing them from accumulating in the brain, he said.
For this study, Mamo and his colleagues used mice capable of producing human amyloid-beta in their livers.
In the mice, the researchers saw that the protein was carried in the blood by triglyceride-rich lipoproteins, which are also produced by the liver, to the brain, just as they do in humans.
Triglyceride-rich lipoproteins are also known to spread triglycerides, a type of cholesterol, from the digestive system to the bloodstream, where it travels throughout the body, potentially damaging organs such as the brain and heart.
Mice with high levels of both amyloid and triglyceride-rich lipoproteins experienced neurodegeneration -- or the loss of structure and function of brain cells -- and brain atrophy, or wasting away, according to the researchers.
This brain atrophy was accompanied by inflammation in the nerves, arteries and veins in the brain, and damage to the cerebral capillaries, which are commonly observed in people with Alzheimer's disease.
Affected mice performed poorly on a learning test that depends on function of the hippocampus, the part of the brain that is essential for the formation of new memories.
The findings, researchers said, will need to be confirmed in human studies before they can be used to shape Alzheimer's prevention and treatment strategies.
However, researchers in Australia have already started the first human study of a drug designed to slow development of amyloid fat proteins in the liver, according to Mamo.
"Disturbances of brain capillaries is the first indication of Alzheimer's disease, preceding cognitive decline by many years," Mamo said.
"Identifying what causes the damage to capillaries and preventing this from occurring notionally could have a dramatic impact for onset and progression of Alzheimer's," he said.