A new study by the University of Colorado Anschutz Medical Campus demonstrates viruses can inflame and disrupt connections between the olfactory system, and the part of the brain associated with memory and learning, which may accelerate the onset of Alzheimer’s disease (AD).

The findings, “Signatures for Viral Infection and Inflammation in the Proximal Olfactory System in Familial Alzheimer’s Disease,” are published in the journal Neurobiology of Aging.

“We know that one of the early signs of Alzheimer’s disease is losing the sense of smell,” explained the study’s lead author Andrew Bubak, PhD, assistant research professor in the division of neurology at the University of Colorado School of Medicine.

The researchers focused on the olfactory tract, olfactory bulb, and the hippocampus. They examined messenger RNA in the brain tissue of six individuals from Colombia who had familial Alzheimer’s disease (FAD) and tissue from a control group without AD. They found signatures of viral infection in the olfactory bulbs of the FAD group and inflammation in the olfactory tract which carries information to the hippocampus. They also discovered altered myelination in the olfactory tract. Myelin is a protective fatty layer around nerves that allows electrical impulses to move quickly and smoothly. If it’s damaged, signaling stalls.

“These findings raise the possibility that viral infection and associated inflammation and dysregulation of myelination of the olfactory system may disrupt hippocampal function, contributing to the acceleration of FAD progression,” the study said.

The study’s senior author, Diego Restrepo, PhD, professor of cell and developmental biology at the University of Colorado School of Medicine, said viruses have long been suspected of playing a role in cognition problems. “Our hypothesis is that some viruses accelerate Alzheimer’s disease,” Restrepo said. “Does the loss of smell specifically accelerate Alzheimer’s? That’s the question.”

“The whole olfactory pathway goes to the hippocampus. If you decrease the signaling along that pathway then you get less signaling to the hippocampus,” Bubak said. “If you don’t use it, you lose it.”

The researchers hope to next focus on better understanding the relationship between the olfactory system and the hippocampus in the context of viral susceptibility and neurodegeneration.

The new study may pave the way for the development of new therapies that detect Alzheimer’s disease earlier and helps illuminate the role that viruses and the olfactory system play in driving the illness.

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