ATMOSPHERE - Alzheimer’s is a devastating disease that destroys brain cells, wiping out memories and cognitive function along the way. While 5.8 million Americans live with the condition today, that number is expected to soar to almost 14 million by 2050, according to the Alzheimer’s Association.
With no cure in sight or even a way to slow the disease’s progression, many researchers are focused on determining what causes Alzheimer’s, hoping to find ways to prevent the disease. In the past 20 years, studies have shown that the brain’s immune system may play a role in the development of Alzheimer’s.
The July 2019 Alzheimer’s Association International Conference, held in Los Angeles, brought together a panel of five experts in this field of research to discuss how treating infections that attack the immune system may slow or prevent the disease — a concept that is vigorously debated among scientists.
“We’re seeing new research in the field that is looking at whether or not a microbe — like a bacteria, virus, or fungus — could be part of the mechanism for the biological changes associated with Alzheimer’s disease,” says Rebecca Edelmayer, PhD, the director of scientific engagement at the Alzheimer’s Association.
“We know that the brain has a very elegant immune system,” Dr. Edelmayer says, but “the idea that infectious agents could be causing something like Alzheimer’s disease or other dementias is still not completely accepted by the research community.”
Is Beta-Amyloid Buildup an Immune Response?
Over the past few decades, investigations have indicated that the buildup and clumping in the brain of a protein called beta-amyloid may be a main culprit in causing Alzheimer’s disease.
But what causes the abnormal levels of beta-amyloid in the first place?
Robert Moir, PhD, an assistant professor in the neurology, genetics, and aging research unit at Massachusetts General Hospital Institute for Neurodegenerative Disease in Boston, has been leading research demonstrating that the protein may actually be part of the immune system.
According to his findings, beta-amyloid (also called amyloid beta) belongs to a family of immune proteins called antimicrobial peptides, which are natural antibiotics and immunomodulators (agents to help normalize or regulate the immune system).
“[These proteins] act as the foot soldiers of innate immunity,” says Dr. Moir, who discussed the topic at the AAIC. “Moreover, amyloid beta protein protects the brain against infection by entrapping invading microbes within amyloid deposits.”
Moir suspects that things go wrong when the brain starts making too much amyloid beta, which then destroys brain cells and leads to dementia.
He and his colleagues are continuing to investigate if amyloid plaques may be a genuine immune response to some type of infection in the brain.
Potential Links Between Herpesviruses and Dementia
Herpes is one of the world’s most common viruses. Herpes simplex virus type 1 (HSV-1), which is best known for causing cold sores, affects about half of Americans ages 14 to 49, according to the American Sexual Health Association.
Ruth Frances Itzhaki, PhD, a professor of biology and health at the University of Manchester in England, suspects that the virus may be a major contributor to Alzheimer’s.
At the AAIC, Dr. Itzhaki discussed her research, published in October 2018 in Frontiers in Aging Neuroscience, which found that HSV-1 enters the brains of many elderly people as their immune systems decline with age.
“It then establishes a latent [dormant] infection, from which it is reactivated by events such as stress, a reduced immune system, and brain inflammation induced by infection by other microbes,” she said in a statement. “Reactivation leads to direct viral damage in infected cells and to viral-induced inflammation."
In experiments with antiviral agents, Itzhaki and her team have found that these therapies may be effective in slowing the progression of Alzheimer’s and may lead the way to dementia prevention by one day creating a vaccination against the herpesvirus.
Ben Readhead, MBBS, an assistant professor at Arizona State University’s Banner Neurodegenerative Disease Research Center in Tempe, also discussed research pubished in July 2018 in Neuron connecting herpesviruses to Alzheimer’s. Dr. Readhead and his colleagues have observed that the brains of Alzheimer’s patients have an abundance of various strains of the herpesvirus, including HHV-6A, HHV-6B, HSV-1, and HHV-7.[EDH]