SARS-CoV-2 infects neurons and induces neuroinflammation in a non-human primate model of COVID-19, 2022, Beckman et al

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9554328/
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiologic agent of coronavirus disease 2019 (COVID-19), can induce a plethora of neurological complications in some patients. However, it is still under debate whether SARS-CoV-2 directly infects the brain or whether CNS sequelae result from systemic inflammatory responses triggered in the periphery.

By using high-resolution microscopy, we investigated whether SARS-CoV-2 reaches the brain and how viral neurotropism can be modulated by aging in a non-human primate model of COVID-19. Seven days after infection, SARS-CoV-2 was detected in the olfactory cortex and interconnected regions and was accompanied by robust neuroinflammation and neuronal damage exacerbated in aged, diabetic animals. Our study provides an initial framework for identifying the molecular and cellular mechanisms underlying SARS-CoV-2 neurological complications, which will be essential to reducing both the short- and long-term burden of COVID-19.

 

I think this abstract rather obscures the significant finding of brain infection in both young healthy and older diabetic monkeys. We've seen brain infection also reported from postmortem studies of human brains.

This study is explained in this readable article:
SARS-CoV-2 causes neuronal damage and inflammation within a week of infection in rhesus macaques

So, my interpretation of this is that the viral infection caused brain damage, making the similarities between some post-viral conditions with traumatic brain injury understandable, and making sense of the increased rates of diagnosis of dementia and cognitive difficulties that have been found in analyses of big medical records databases.

I think this team is one to watch, to see what they make of longer term impacts of covid-19 on the monkeys.