COVID-19 and the brain

Although SARS-CoV-2 probably does not infect the brain, it can damage it significantly, a new study of autopsies of 41 COVID-19 patients finds.

Researchers at Columbia University say that they found no signs of virus inside the patients' brain cells but saw many brain abnormalities that could explain the confusion and delirium seen in some patients with severe coronavirus and the lingering "brain fog" in those with mild disease.

The study, which the authors called the largest COVID-19 brain autopsy report thus far, involved analysis of samples from autopsies conducted from March to June 2020 and was published late last week in Brain. The findings, they said, suggest that the inflammation triggered by the coronavirus in other parts of the body or in the brain's blood vessels may have caused the neurologic abnormalities seen in the autopsies.

Lack of oxygen, cell death

The brain damage consisted of areas starved of oxygen, many of them hemorrhagic, which the researchers said were likely caused by blood clots that temporarily blocked the flow of oxygen. Many activated microglia, or immune cells in the brain that can be activated by pathogens, were also identified.

"We found clusters of microglia attacking neurons, a process called 'neuronophagia,'" co-senior author Peter Canoll, MD, PhD, said in a Columbia University press release.

Because no virus was observed in the brain, he said that the microglia may have been activated by inflammatory cytokines, which are tied to coronavirus infection. "At the same time, hypoxia [reduced oxygen from COVID-19] can induce the expression of 'eat me' signals on the surface of neurons, making hypoxic neurons more vulnerable to activated microglia."

Most activated microglia were found in the lower brain stem, which is responsible for heart and breathing rhythms and levels of consciousness, and in the hippocampus, which is involved in mood and memory.

"We know the microglia activity will lead to loss of neurons, and that loss is permanent," co-senior author James Goldman, MD, PhD, said in the release. "Is there enough loss of neurons in the hippocampus to cause memory problems? Or in other parts of the brain that help direct our attention? It's possible, but we really don't know at this point."

Understanding cellular and molecular aspects of COVID-19 brain damage could direct interventions to reduce long-term NPs. Interventions may involve antagonists of cytokines (etanercept, infliximab), NMDA receptor (ketamine), TNF-α and anti-inflammatory pathways (aspirin, celecoxib), and kynurenine pathway modulators (minocycline).3 Mitigating long-term post–COVID-19 cognitive, emotional, and behavioral sequelae would decrease disease burden. COVID-19 neuropathology may serve as a model for deciphering neurodegenerative processes related to neuroinflammation in other brain diseases and developing new treatment strategies.

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Regards,

Nancy Ella