Resume: The onset of Alzheimer’s disease may be hastened by viruses that inflame and disrupt olfactory system signals to the hippocampus, a new study reports.
Fountain: colorado university
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 at the University of Colorado. Anschutz Medical Campus.
The findings, published 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.
Bubak’s team 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 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 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.
Bubak’s team focused on the olfactory tract, the olfactory bulb, and the hippocampus, the area of the brain that manages memory and learning. The image is in the public domain.
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.”
Bubak and Restrepo suspect 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.
About this Alzheimer’s disease research news
Author: David Kelly
Fountain: colorado university
Contact: Press Office – University of Colorado
Picture: The image is in the public domain.
See also
original research: Open access.
“Signatures of viral infection and inflammation in the proximal olfactory system in familial Alzheimer’s disease” by Andrew Bubak et al. neurobiology of aging
Abstract
Signatures of viral infection and inflammation in the proximal olfactory system in familial Alzheimer’s disease
Alzheimer’s disease (AD) is characterized by deficits in smell and olfactory pathology that precedes the diagnosis of dementia.
Here we analyze differential gene and protein expression in the olfactory bulb (OB) and tract (OT) of individuals with familial AD (FAD) who carry the autosomal dominant presenilin 1 E280A mutation. Compared to control, FAD OT had increased immunostaining for amyloid β (Aβ) and CD68 in high and low myelin regions, as well as increased immunostaining for Iba1 in the high myelin region.
In FAD samples, RNA sequencing showed: (1) viral infection in the OB; (2) inflammation in the OT that carries information via the entorhinal cortex from the OB to the hippocampus, a brain region essential for learning and memory; and (3) decreased oligodendrocyte deconvoluted transcripts.
Interestingly, spatial proteomic analysis confirmed impaired myelination in the OT of individuals with FAD, implying dysfunction of OB-hippocampal communication.
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.
Source: news.google.com