Viruses can inflame and disrupt connections between the olfactory system, which governs the sense of smell, and the part of the brain associated with memory and learning, possibly accelerating the onset of Alzheimer’s disease, according to a new study from researchers of the University of Colorado Anschutz Medical Campus.
The recommendationspublished Tuesday in the journal Neurobiology of Aging, could lead to new therapies that detect Alzheimer’s disease (AD) earlier while helping to illuminate the role viruses and the olfactory system play in driving the disease.
“We know that one of the earliest signs of Alzheimer’s disease is loss of the sense of smell,” said study lead author Andrew Bubak, PhD, a research assistant professor in the division of neurology at the University of California School of Medicine. University of Colorado.
The researchers focused on the olfactory tract, the olfactory bulb, and the hippocampus, the area of the brain that manages memory and learning.
They examined messenger RNA in brain tissue from six people 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 that carries information to the hippocampus. They also discovered impaired myelination in the olfactory tract. Myelin is a protective fatty layer around nerves that allows electrical impulses to move quickly and smoothly. If it is damaged, the signaling stops.
“These findings raise the possibility that viral infection and associated inflammation and dysregulation of myelination of the olfactory system may alter hippocampal function, contributing to the acceleration of FAD progression,” the study said.
The study’s lead authors, Maria Nagel, MD, a research professor of neurology and Diego Restrepo, PhD, a professor of cell and developmental biology at the CU School of Medicine, said viruses have long been suspected of playing a role in cognitive problems. Some studies have associated the SARS-CoV-2 virus, which causes COVID-19, with dementia. The virus, which travels through the nose, causes some of those infected to lose their sense of smell.
At the same time, the varicella zoster virus that causes herpes zoster and the herpes simplex virus can deposit amyloid beta, a protein essential for the development of AD, in the olfactory bulb. Viruses often persist for years even after symptoms have disappeared.
“Our hypothesis is that some viruses accelerate Alzheimer’s disease,” Restrepo said. “Does loss of smell specifically accelerate Alzheimer’s? That is the question.”
The researchers suspect that inflammation and amyloid deposits in the olfactory system disrupt communication with the hippocampus. Without sensory input, they believe, the hippocampus begins to degenerate.
“The entire olfactory pathway goes to the hippocampus. If you decrease signaling along that pathway, then you get less signaling in 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.
Study co-authors include Laetitia Merle, Christy S. Niemeyer, B. Dnate’ Baxter, Adrianna Gentile Polese, Vijay Ramakrishna, Johanna Gomez, Lucia Madrigal, Andres Villegas-Lanau, Francisco Lopera, Wendy Macklin, and Seth Frietze.
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