Neuroinvasion is the techical name for this avenue of infection. In this case, the virus can travel directly up the nose, via what are known as sustenacular cells, to the olfactory bulb. Then, it can replicate or ride synapses up the olfactory nerve to central parts of the brain, potentially.
UC Davis publicized a statement about the research, which was published in Cell Reports. The statement included the following:
Using a recently developed nonhuman primate model of the disease, UC Davis researchers revealed that COVID reaches the brain by transport through the nose along the olfactory nerve, a nerve that starts in the brain and ends in the upper inside part of the nose.
“We not only demonstrated that the virus infects the brain, but also that it directly infects neurons and can be transported along nerve pathways to sites beyond the initial olfactory regions,” said senior author John Morrison, professor of neurology at UC Davis and director of the CNPRC [California National Primate Research Center].
[…]
Their findings leave no doubt that the virus was entering the brain and damaging brain cells along the way, said first author Danielle Beckman, a postdoctoral researcher at UC Davis. By comparing young and aged animals, it became clear that viral infection was exacerbated in the aged animals. Brain cells of infected aged monkeys appeared shrunken.
This is important because of the neurocytoarchitectural areas to which the olfactory bulb connect. One of those structures may be very familiar to you: the amygdala, also known as the “fear center” of the brain. (Really, it’s designed to detect threat; fear is a body state, not an environmental cue.)
Other vital connecting areas are those that, along with the amygdala, go on to help encode memory. This is why many researchers have sounded the alarm that Long Covid may produce its own version of dementia, on the order of Alzheimer’s if not triggering Alzheimer’s itself:
Perhaps most striking was the distance the virus traveled in aged animals compared to the young, healthy animals. While the virus was mostly found in the primary olfactory cortex in all inoculated animals, the virus spread further in aged animals. Cellular markers of SARS-CoV-2 were seen in regions of the brain extending beyond immediate sensation and perception of smell, and into areas highly involved in emotion, memory and cognition in aged animals. These findings raise concerns about potential spikes in neurodegenerative diseases and vulnerability to dementia-related illnesses, like Alzheimer’s, as infected adults age.
“In the aged monkeys in particular, the virus is infecting neurons in regions known to be highly vulnerable to Alzheimer’s disease,” Morrison said.
(Emphases added.)
Now, what was the culprit: the virus itself or the inflammation as a downstream process? It appears that still needs to be teased out, but suffice to say that both could be occurring simultaneously; it doesn’t have to be one or the other. But the study showed that “the intensity with which SARS-CoV-2 induced inflammation in aged rhesus macaques led to significant damage,” according to one researcher.
I plan to write far more on this in the near future, but I wanted to get this stub of an article up quickly so as to give people more information, more ways for all of us to arm ourselves. These results are all the more reason to keep masking! Get boosted (that is, if your doctor does not feel that it would be contraindicated); but also protect your airways! Keep that critter out of the nose.
Edited to thank this is only a test for a crucial correction to the link to the study.