A Yale-led study has found strong evidence that, in at least a subset of people with long COVID, the immune system may be attacking the body’s own brain and nerve tissues. The findings, published in CELL, could help explain why some patients have brain fog, dizziness, headaches, fatigue, burning pain and numbness.
That is why the study is drawing attention now. Six years after COVID-19 first swept the world, long COVID remains one of the pandemic’s most stubborn aftereffects, with symptoms that can linger long after the initial infection and vary so widely from patient to patient that doctors have struggled to pin down a single cause. For people still searching for a long covid treatment, the new work offers a biologic lead rather than another list of symptoms.
The research team analyzed blood samples from people with long COVID, healthy volunteers and people who recovered from COVID without lasting symptoms. It then purified antibodies from patients’ blood and exposed them to brain and nerve tissues. In many long COVID patients, the autoantibodies appeared to target parts of the brain and nervous system involved in pain signaling, memory, balance, sensory processing and autonomic nervous system control. Akiko Iwasaki, who co-led the work at Yale and has spent years studying the condition in her lab, said the result points to one possible mechanism that could help explain a subset of cases.
Iwasaki also said the finding does not explain the entire long COVID scenario. That matters because the study’s autoimmune signal appears only in some patients, not all, and long COVID has no single known fingerprint. The condition may overlap with autoimmune disease, but it does not perfectly resemble any known autoimmune disorder, which leaves the hardest clinical question unanswered: which patients would actually qualify for therapies aimed at calming an autoimmune attack?
The research included a Mount Sinai Health System team led by David Putrino, a professor of rehabilitation and human performance and the Nash Family Director of the Cohen Center for Recovery from Complex Chronic Illness. The researchers said the work could eventually point toward treatments already used for other autoimmune diseases, but only if the findings are validated and the right patients can be identified.
For now, the most consequential next step is not a new drug. It is proving which long COVID patients share this immune pattern, and whether those patients improve when the immune attack is treated. Without that, the study remains an important clue — and not yet a prescription.
