Research from a clinical study implied that patients who recovered from COVID infection had brief or even lasting cognitive impairment. Typical symptoms were deficits in executive functioning, processing speed, attention, memory, and language, which are together called ‘Brain fog’. This adds significantly to the morbidity of post–COVID-19 conditions (also named as 'long COVID') along with increased incidence of depression, anxiety, sleep disorder and tiredness.

As there is a lack of neurocognitive longitudinal studies on post-COVID brain fog and the hesitation of doctors to accept this condition as an organic disorder without a pathobiological notion. So, Anthony Fernandez-Castaneda and associates investigated how mild respiratory infections could lead to neuroinflammation and subsequent brain impairment.

These researchers demonstrated mild respiratory COVID in a mouse. No SARS-CoV-2 in the brain was detected. Researchers witnessed signs of inflammation in the cerebrospinal fluid and serum, that triggered resident macrophage cells (called as microglia) in the hippocampal and subcortical white-matter areas. Interestingly, a small number of patients with SARS-CoV-2 infection and no substantial lung dysfunction at the time of death had similar outcomes.

Microglia activation seemed to be mediated by constantly raised levels of C-C motif chemokine 11 (CCL11). This anti-microbial gene has been linked with ageing and inhibition of neurogenesis. Hence, the people with long COVID and cognitive deficiencies had raised values of serum CCL11 compared to those with long COVID with no cognitive signs.

These findings can serve as the basis for the management of neurologic and psychiatric symptoms of long COVID. Various drugs concentrating on the activation of microglia have been assessed in the preclinical models of identical syndromes of cognitive dysfunction. Some NSAIDs, tetracyclines and FDA-approved inhibitors of the colony-stimulating factor 1 (CSF1) receptor i.e. Pexidartinib used for symptomatic rare benign tumours can help to lessen microglia.

These findings support the assessment of microglial modulators for the treatment of COVID-related brain fog. Also, CCL11 could be an effective target and a candidate biomarker. Although the conclusions of brain dysfunction and patterns of damage during and after COVID are daunting because of the resemblances with changes in neurodegenerative disorders, translational research like this one may direct towards precise diagnoses and therapies for cognitive dysfunction after COVID.