August 11, 2016
A provocative new study posits the theory that Alzheimer’s disease may be a response to infection in the brain. It will require far more study to determine whether infections play a role in Alzheimer’s disease, but the findings underscore how much scientists still need to learn about the causes of Alzheimer’s and the factors that may aggravate the disease. Such research will help doctors better understand Alzheimer’s, and indirectly may help them to design more effective strategies to treat or even cure the illness.
The new study, from researchers at Harvard, suggests that Alzheimer’s may result from the brain’s attempt to fight off some kind of infectious organism,perhaps a virus or bacteria,that enters the brain. The immune system, according to this theory, responds by producing sticky proteins called beta-amyloid that encase the invading organism, causing it to die.
The buildup of beta-amyloid in the brain is a hallmark of Alzheimer’s disease, causing amyloid plaques to form and accumulate outside brain cells. But whether amyloid plaques are a cause or an effect of Alzheimer’s remains largely debated.
This new theory proposes that beta-amyloid may be an immune system response to infections. Mice that had Salmonella bacteria injected into their brains, for example, responded by forming beta-amyloid plaques. Human brain cells cultured in the laboratory showed a similar response to yeast infections. Other research has pointed to similar responses to infection with the flu and herpes viruses.
“Our findings raise the intriguing possibility that Alzheimer’s pathology may arise when the brain perceives itself to be under attack from invading pathogens,” said study author Robert Moir of Harvard Medical School and Massachusetts General Hospital. “Further study will be required to determine whether or not a bona fide infection is involved.”
Normally, the brain is protected against infections and other toxins by something called the blood-brain barrier. Oxygen and nutrients can enter the brain, but viruses, bacteria and other threats are kept out.
But as we age, the blood-brain barrier begins to break down, allowing infections and other toxins from the blood to enter the brain. According to the new theory, this breakdown in the blood-brain barrier could play a role in the onset of Alzheimer’s. The findings were published in the journal Science Translational Medicine.
In another study, published in the journal Radiology, researchers in the Netherlands used MRI brain scans to measure the blood-brain barrier in 16 people with early Alzheimer’s and 17 healthy peers. They found that the blood-brain barrier was considerably more leaky in those with early Alzheimer’s compared to that in the healthy controls.In addition, the greater the decline in thinking and memory skills among those with Alzheimer’s, the researchers found, the greater the leakage in the blood-brain barrier.
The findings, they say, suggest that a leaky blood-brain barrier may be an early step in the progression to Alzheimer’s disease. But much more work needs to be done to determine whether infection plays a role in that process.
The findings highlight how much scientists still don’t know about the causes of Alzheimer’s disease. Only through continued basic research into the fundamental underpinnings of Alzheimer’s will better ways to prevent or treat the disease become available.
By www.ALZinfo.org, The Alzheimer’s Information Site. Reviewed by Marc Flajolet, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.
Sources:Deepak Kumar Vijaya Kumar, Se Hoon Choi, Kevin J. Washicosky, et al: “Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer’s disease.” Science Translational Medicine, May 25, 2016
Harm J. van de Haar, M.Sc., SaartjeBurgmans, Ph.D., Jacobus F. A., et al: “Blood-Brain Barrier Leakage in Patients with Early Alzheimer Disease.” Radiology, June 1, 2016.