Viruses have accelerated the development of Alzheimer’s disease by damaging the olfactory system

(ORDO NEWS) — A new paper has shed light on the link between viral infections, smell perception and Alzheimer’s disease.

It turned out that, in addition to local inflammation in the olfactory system and the accumulation of toxic beta-amyloid, viruses are to blame for the degradation of the hippocampus – an important part of the brain with many functions – due to a decrease in the signals it receives.

Viruses can ruin a person’s life great, acting on different organs and systems through various mechanisms. In particular, they can trigger inflammatory reactions, both systemic and local.

Among other things, viruses can disrupt the human olfactory system. The most topical (although not the only) example is the SARS-CoV-2 coronavirus, the causative agent of the dangerous Covid-19 infection and the culprit of the pandemic. The disease often causes changes in the olfactory bulbs and loss of the sense of smell.

Notably, odor sensitivity is also severely affected in Alzheimer’s disease . Moreover, a noticeable deterioration in the sense of smell serves as an early diagnostic sign of neurodegeneration.

Recall that Alzheimer’s disease is the most common neurodegenerative disease. It leads to accelerated death of nerve cells associated with progressive impairment of memory and cognitive functions. In this case, it is the hippocampus that suffers especially strongly, as well as certain parts of the cerebral cortex.

Employees of the University of Colorado (USA) addressed the difficult question of the connection between nerve cells, smell and viruses. They examined the components of the olfactory system – the olfactory bulbs, the olfactory tract and the hippocampus.

It is worth recalling that the role of the hippocampus is not limited to the perception of smells – it is an important part of the brain responsible for learning and memory.

The subjects were six patients who were diagnosed with a familial form of Alzheimer ‘s disease, as well as healthy people from the control group. For each, scientists analyzed the proteome (the totality of proteins in the cell) and transcriptome (the composition of messenger RNA).

It turned out that with a viral infection, gene expression in the olfactory bulbs changes in a special way – and only in the case of patients with Alzheimer’s disease. At the same time, the olfactory tract of such people (which connects the olfactory bulbs and the hippocampus) becomes inflamed.

In addition, myelination is disrupted in this part of the brain – the process of forming an “insulating winding” around the nerve fibers, due to which the impulse spreads through them faster.

The next important factor in the “vicious” connection of viruses with neurodegeneration is the deposition of beta-amyloid.

This is a protein fragment that plays an important role in the development of Alzheimer’s disease, especially in its onset. Beta-amyloid accumulates in large quantities in the brain, where it forms toxic aggregates of various sizes.

The varicella-zoster virus and the herpes simplex virus are known to contribute to the accumulation of “deposits” of beta-amyloid.

“According to our hypothesis, some viruses accelerate the development of Alzheimer’s disease,” said Diego Restrepo, one of the authors of the new article, “But does the loss of smell accelerate Alzheimer’s disease? That’s the question.”

Scientists quite reasonably assume that the disruption of communication between the hippocampus and the olfactory bulbs (which is just caused by inflammation and amyloid beta) triggers the functional degradation of the hippocampus.

Receiving fewer and fewer signals from the outside, it begins to work worse and gradually collapses.

“What you don’t use, you invariably lose” is the main conclusion of the study in a nutshell.

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