The article reports that researchers are uncovering long-term neurological effects of SARS-CoV-2, suggesting Covid-19 can disrupt and potentially damage the brain, not just the lungs.
Early in the pandemic, Avindra Nath of the National Institute of Neurological Disorders and Stroke investigated unexplained deaths in New York in which victims stopped breathing without lung or heart damage. High-resolution imaging and microscopic examination revealed loss of neurons in brain stem regions that control breathing. Later, recovering patients described episodes in which breathing no longer felt automatic, resembling Ondine’s curse.
As the pandemic progressed, clinics filled with patients whose initial respiratory symptoms had resolved but who experienced persistent fatigue, cognitive slowing, malaise and other symptoms. Many cases overlapped with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), and later studies found a substantial share of long-Covid patients met ME/CFS diagnostic criteria. Damage in the brain stem and surrounding tissue may interfere with thinking, mood and regulation of heart rate, digestion and blood pressure.
Long Covid has risen rapidly in diagnoses and become economically disruptive. A December study estimated up to 400 million people worldwide are living with long-term consequences of infection, and a November analysis put the annual global economic toll at $1 trillion.
Research increasingly links Covid to structural and cognitive changes in the brain. UK Biobank scans showed subtle loss in regions involved in planning and memory, even after mild infections, along with small declines in cognitive scores in community studies. Although risks appear lower after vaccination and milder infections, they have not disappeared.
In a UK human challenge study, healthy young adults infected with the original strain performed slightly worse a year later on memory and decision-making tests—about a six-point IQ difference—despite mild illness and no reported lasting problems. Observational research and large datasets have found higher risks of cognitive impairment and, in older adults, dementia-level decline months or years after infection.
Older adults and those severely ill appear most affected. Blood tests have revealed proteins linked to Alzheimer’s disease, including phosphorylated tau, particularly in patients with persistent neurological symptoms. A study from NYU Langone Health found enlargement and impaired blood flow in a brain structure involved in immune regulation and waste clearance, along with Alzheimer’s-linked blood markers.
While some researchers caution that biomarkers do not guarantee dementia, Nath argues Covid can accelerate neurodegenerative processes already underway in aging populations. Korean researchers reported structural and biochemical changes about a year after mostly mild infections in patients with lingering cognitive problems, including thinner brain regions tied to attention and memory, iron buildup, enlargement of a structure involved in immune regulation and waste clearance, and blood markers of ongoing brain stress and injury. These findings were replicated in a separate group.
The emerging picture is of subtle but widespread cognitive effects that may erode independence and productivity over time. Nath is leading a clinical trial at the NIH treating long Covid as an immune-driven neurological condition, testing whether immunomodulating therapies can reduce lingering inflammation and restore function. The study is expected to conclude later this year.
