Brain fog after COVID-19? Study shows severe infection can trigger expression of ‘old age’ genes

The impact of COVID-19 on the human brain piqued the curiosity of the scientific community and the general public alike since the first year of the pandemic. A new study done over almost two years can shed light on post-COVID-19 neurological conditions such as ‘brain fog’. 

Changes in the gene activity in the brain of people with severe COVID-19 were found to be similar to that seen in old age, according to a new study.

Genes that are expressed in the brains of older people were seen active in COVID-19 patients who had to be admitted to the intensive care unit (ICU) and needed ventilator support, the analysis of post-mortem reports of brain samples showed. 

This may be linked to the decline in cognitive abilities experienced by several patients after a severe SARS-CoV-2 infection, the report published December 5, 2022 in the journal Nature Ageing noted. 

The study was carried out by Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, and her colleagues. They compared brain samples of COVID-19 patients with those of people who never contracted the infection. 

The samples of the frontal cortex — a region in the brain majorly responsible for cognition — were from:   

• Twenty-one patients who died of severe COVID-19 
• One who died of asymptomatic COVID-19 infection 
• Twenty-two people with no history of COVID-19 
• Nine people who never had COVID-19 but were subjected to medical interventions similar to severe COVID-19 patients, such as ventilator support or ICU treatment, which can cause serious side-effects 
• Ten uninfected people who died at the age of 38 years or younger
• Ten uninfected people who were 71 years or older

Genes that are linked to inflammation and stress were expressed more in the brains of people with severe COVID-19 than in the others, the scientists found. “Conversely, genes linked to cognition and the formation of connections between brain cells were less active.”

The comparison of the samples from the age-controlled groups showed that changes in the brain of older people were mirrored in those with severe COVID-19.

The changes in brain gene activity were also more pronounced in patients with severe COVID-19 than in uninfected controls who required critical care and ventilator support, according to the report. 

There is a growing body of research on how brain functions are affected by COVID-19 infection, causing memory loss, prolonged loss of smell and taste, insomnia as well as other neurological symptoms experienced worldwide by people who recovered from the infection.

One such study published in JAMA Network in May 2021 showed that 80 per cent of the patients hospitalised with COVID-19 had some neurological manifestation. 

The most common self-reported symptoms included headache (37 per cent) and loss of smell or taste (26 per cent), the research done on 3,744 patients showed. “The most common neurological signs and / or syndromes were acute encephalopathy (49 per cent), coma (17 per cent) and stroke (6 per cent),” the report by a group of American and European scientists stated. 

A July 2021 review report of existing literature on the topic — that inspired Mavrikaki to begin her research — indicated that SARS-CoV-2 “might attack certain brain cells directly, reduce blood flow to brain tissue or trigger production of immune molecules that can harm brain cells”. 

The report, however, incorporated studies that indicated the virus may not be abundantly present in the brain and doesn’t attack neurons in any significant way. 

But earlier as well as later studies suggested otherwise. A January 2021 research done on mice infected with COVID-19 found that the peak viral load in the brain was 1,000 times greater than in the lungs. 

Another report published in the journal Molecular Psychiatry November 1, 2022 showed why COVID-19 patients are at a higher risk on neurodegenerative diseases such as Parkinson’s and Alzheimer’s. 

The SARS-CoV-2 virus triggered microglia, the brain’s immune cells, “activating the same pathway that Parkinson’s and Alzheimer’s proteins can activate”, it showed. 

Inflammation, rather than virus infiltration in the brain, was more likely to be responsible for altered gene expression during COVID-19, Mavrikaki and her team found. 

To arrive at this observation, the scientists exposed laboratory-cultured neurons to proteins that promote inflammation. The activity of a subset of aging-related genes in the brain changed as a result, they noted. 

Several questions still remain, the authors noted. Further research is needed to establish the role of comorbidities caused by conditions such as obesity and the impact of COVID-19 in the brain of patients with milder and other infections, they added. 

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