News Health Covid survivors with depression show signs of brain inflammation, claims study

Covid survivors with depression show signs of brain inflammation, claims study

Translocator protein volume in the brain regions of interest was higher in participants with depressive and cognitive symptoms than in controls (17 per cent).

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Patients with persistent symptoms of depression and cognitive impairment, after a mild to moderate Covid-19 infection, had elevated levels of a protein indicating inflammation of the brain, according to a study. Prolonged symptoms of Covid-19 have been found in many patients, often known as long Covid. Psychiatric symptoms like anxiety and depression are the most common and could last for weeks, even months, after recovery.

Researchers from the Centre for Addiction and Mental Health in Canada used positron emission tomography (PET) to compare levels of translocator protein -- a marker for gliosis (inflammation of the brain), in 20 participants with persistent symptoms of depression and cognitive impairment with those of 20 healthy controls.

The results, published in JAMA Psychiatry, showed that Translocator protein volume in the brain regions of interest was higher in participants with depressive and cognitive symptoms than in controls (17 per cent). The difference was most pronounced in two regions of the brain: the ventral striatum (22 per cent) and dorsal putamen (20 per cent).

"Gliosis may be consequent to inflammation, injury, or both, particularly in the ventral striatum and dorsal putamen, which may explain some persistent depressive and cognitive symptoms, including slowed motor speed, low motivation or energy, and anhedonia (reduced ability to experience pleasure)," the researchers said.

In a related commentary, Alexander Gerhard, of the University of Manchester in UK, said the study was limited by PET's signal, which is not restricted to microglial cells. "To target neuroinflammatory changes therapeutically, we will need a much more detailed understanding of microglial activation at different time points of neurological disorders," Gerhard wrote.

"Not surprisingly, relatively simplistic attempts to suppress microglial activation have so far not resulted in clinical meaningful results."