The olfactory system, which regulates sense of smell, and the part of the brain associated with memory and learning can get irritated and disrupted by viruses, thus hastening the onset of Alzheimer's disease.
A recent study from scientists at the University of Colorado Anschutz Medical Campus suggests that viruses may cause inflammation and damage to the connections between the olfactory system and the hippocamus. This will hasten the development of Alzheimer’s disease. The sensory system used for scent is called the olfactory system. The hippocampus governs memory and learning. It is thought to be affected by the disruption of the olfactory tract, according to CU Anschutz researchers.
â€œWe know that one of the early signs of Alzheimerâ€™s disease is losing the sense of smell,â€ said lead author Andrew Bubak, PhD at the University of Colorado School of Medicine.
The research was published in the journal Neurobiology of Aging.
It may help develop new treatments for Alzheimer’s disease (AD) and give light on how viruses and the olfactory system contribute to the illness.
Olfactory viral inflammation and Alzheimer’s :
A major obstacle to treating AD is the long time lag between the development of AD and diagnosis.
In order to stop the progression of the disease to alzheimer, doctors must be able to diagnose AD early.
A loss of smell is a first stage of AD, occurring before clinical dementia.
The olfactory tract, olfactory bulb, and hippocampus, the part of the brain that controls memory and learning, were the focus of Bubak’s research team.
The team looked at messenger RNA in brain tissue from a control group of people without Alzheimer’s disease. They collected tissue from six people from Colombia who had the familial form of the disease (FAD).
The FAD group’s olfactory bulbs and the olfactory tract both showed signs of viral infection. In the olfactory tract, they also identified abnormal myelination. A protective fatty layer called myelin surrounds nerves. It enables rapid and fluid electrical impulses. If it is broken, the signalling stops.
Viruses & cognitive illnesses:
The senior authors of the study, Maria Nagel, MD, and Diego Restrepo, PhD, noted that viruses have long been thought to contribute to cognitive issues.
The SARS-CoV-2 virus, which causes COVID-19, has been linked in some studies to dementia.
Some people who contract the virus, which spreads through the nose, lose their ability to smell.
Virueses like herpes simplex, shingles, varicella zoster etc can cause the olfactory bulb to accumulate amyloid beta. The onset of Alzheimer’s disease can be sped up by viruses that irritate and obstruct communication between the olfactory system and brain. Even after symptoms stop, infections can sometimes persist for years.
Role of Inflammation proved:
The team theorises that some viruses hasten the onset of Alzheimer’s. Bubak and Restrepo speculate that inflammation is to blame. Also, the olfactory system’s amyloid deposits interfere with communication with the hippocampus. They contend that when there is no sensory input, the hippocampus starts to deteriorate.
The hippocampus is the final stop on the olfactory route. Less signalling reaches the hippocampus if the signalling along that pathway is reduced. If it goes unused, it is lost.
These results suggest that viral infection accompanies inflammation. This disrupts olfactory system myelination. And also leads to impaired hippocampal function, hastening the onset of AD.
Using novel regional or spatial transcriptomic and proteomic assays, the team were able to determine gene expression changes in FFPE olfactory tissues from control and FAD samples.
The findings reveal a transcriptomic signature for viral infection in the OB. Alongside inflammation and dysregulation of myelination in the OT in FAD samples compared to control samples.
The results were confirmed by proteomic analysis.
Future of the study:
The next area of attention for the researchers will be on gaining a deeper understanding of how the olfactory system and the hippocampus interact in the setting of viral susceptibility and neurodegeneration.