Danger: Disruption of smell and viral inflammation are associated with accelerated onset of Alzheimer's disease

Researchers at CU Anschutz suspect that the virus destroys the olfactory nerve, which in turn affects the hippocampus
, which controls memory and learning.

According to a new study by researchers at the University of Colorado's Ann Schutz School of Medicine, viruses may accelerate the onset
of Alzheimer's disease by triggering inflammation and disrupting connections between the olfactory system that controls smell and parts of the brain related to memory and learning.
        

The findings, published Dec.
13 in the journal Neurobiology of Aging, could lead to new treatments that detect Alzheimer's disease (AD) earlier, while helping to elucidate the role
viruses and olfactory systems play in driving disease progression.

"We know that one of the early symptoms of Alzheimer's disease is loss of smell," said Dr.
Bubak, the study's lead author and assistant research professor in
the Division of Neurology at the University of Colorado School of Medicine.
Bubak's team focused on the olfactory tract, olfactory bulb, and hippocampus, the area of the brain that manages memory and learning
.
        

They examined mRNA in the brain tissue of 6 familial Alzheimer's disease (FAD) patients from Colombia, as well as mRNA
from a control group without AD.
They found features of viral infections in the olfactory bulb of the familial Alzheimer's disease group and inflammation
in the olfactory tract that carries information to the hippocampus.
They also found altered
myelination in the olfactory tract.
The myelin sheath is a protective fat layer around nerves that allows electrical impulses to move
quickly and smoothly.
If damaged, the signal stops
.

The study's senior authors, Maria Nagel, M.
D.
, professor of neurology, and Diego Restrepo, Ph.
D.
, professor of cell and developmental biology at 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 of COVID-19 to dementia
.
The virus spreads through the nose, causing some infected people to lose their sense of
smell.
"These findings raise the possibility that viral infection and associated inflammation, as well as dysmyelination of the olfactory system, may disrupt hippocampal function, thereby accelerating the progression of
FAD.
"

Meanwhile, varicella zoster virus and herpes simplex virus, which cause shingles, can deposit amyloid, a protein
essential for the development of AD, in the olfactory bulb.
Even after the symptoms disappear, these viruses often persist for
years.
        

"Our hypothesis is that some viruses accelerate Alzheimer's," "Does the loss of smell accelerate Alzheimer's?" That's the problem
.
Bubak and Restrepo suspected that amyloid deposition in the inflammatory and olfactory systems interrupted communication
with the hippocampus.
They believe that without sensory input, the hippocampus begins to degenerate
.
"The entire olfactory pathway leads to the hippocampus
.
If you reduce the signals on this pathway, then you send fewer signals to the hippocampus," Bubak said
.
"If you don't use it, you lose it
.
"

The researchers hope to next better understand the relationship between
the olfactory system and the hippocampus in the context of viral susceptibility and neurodegeneration.
Combined with the recent new coronavirus infection, the sense of smell and taste of some patients will be affected in the short term, and the results of this study are even more interesting
.