Viruses can inflame and disrupt connections between the olfactory system, which governs smell, and the part of the brain associated with memory and learning, possibly accelerating the onset of Alzheimer’s disease, according to a researcher. new study from researchers at the University of Colorado. Anschutz Medical Campus.
The findings, published Tuesday in the journal Neurobiology of Aging, might lead to new therapies that detect Alzheimer’s disease (AD) earlier while helping to shed light on the role that viruses and the olfactory system play in driving the disease. sickness.
“We know that one of the first signs of Alzheimer’s disease is loss of smell,” said study lead author Andrew Bubak, PhD, assistant research professor in the Division of Neurology. from the University of Colorado Medical School.
Bubak’s team focused on the olfactory tract, the olfactory bulb and the hippocampus, the area of the brain that handles memory and learning.
They examined messenger RNA in brain tissue from six Colombian people with familial Alzheimer’s disease (FAD) and tissue from a control group without Alzheimer’s disease. They found signatures of viral infection in the FAD group’s olfactory bulbs and inflammation in the olfactory tract that 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 travel quickly and smoothly. If it is damaged, the signaling stops.
“These findings raise the possibility that viral infection and associated inflammation and myelination dysregulation of the olfactory system may disrupt hippocampal function, contributing to accelerated progression of FAD,” the study states.
The study’s lead author, 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 linked the SARS-CoV-2 virus, which causes COVID-19, to dementia. The virus, which spreads through the nose, causes some infected people to lose their sense of smell.
At the same time, the varicella zoster virus that causes shingles and the herpes simplex virus can deposit beta-amyloid, a protein essential for the development of AD, in the olfactory bulb. Viruses often persist for years even following symptoms disappear.
“Our hypothesis is that certain viruses accelerate Alzheimer’s disease,” Restrepo said. “Does loss of smell specifically accelerate Alzheimer’s disease? That’s the question.
Bubak and Restrepo suspect inflammation and amyloid deposits in the olfactory system interrupt 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 this pathway, you get less signaling to the hippocampus. If you don’t use it, you lose it.
Andrew Bubak, PhD, Assistant Research Professor, Division of Neurology, University of Colorado School of Medicine
The researchers then hope to focus on better understanding the relationship between the olfactory system and the hippocampus in the context of viral susceptibility and neurodegeneration.
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Journal reference:
Boubak, A.N., et al. (2022) Signatures of viral infection and inflammation in the proximal olfactory system in familial Alzheimer’s disease. Neurobiology of aging. doi.org/10.1016/j.neurobiolaging.2022.12.004.
