Long COVID antibodies trigger sensory, but not cognitive, deficits in mice

Long COVID antibodies trigger sensory, but not cognitive, deficits in mice

Publication date: Aug 26, 2026

According to a recent report in Acta Neuropathologica, the study investigated the potential role of IgG autoantibodies in neurological long COVID, specifically focusing on pain-related sensory dysfunction. Researchers transferred IgG from 13 adults with long COVID and neurological symptoms into mice, observing a clear effect on sensory sensitivity. The antibodies induced thermal and mechanical hypersensitivity in the mice, demonstrated by increased paw withdrawal times from heat and heightened responses to mechanical stimulation, while no cognitive impairments, anxiety, depression, or fatigue were observed. Importantly, the study found that the antibodies accumulated in the lumbar dorsal root ganglia, clusters of sensory neuron cell bodies, and did not trigger widespread neuroinflammation. These findings suggest an autoimmune component in a subset of long COVID patients experiencing hypersensitivity to touch, heat, or cold, and highlight the need for further research to identify the specific antibody targets involved.

Concepts Keywords
Antibodies
Antibody
Brain
Cognitive
Covid
Hypersensitivity
Igg
Long
Memory
Neurological
Neurons
Pain
Sensory
Sequelae
Symptoms

Semantics

Type Source Name
disease MESH Long COVID
disease MESH inflammation
disease MESH pain
disease MESH hypersensitivity
disease MESH cognitive impairment
disease MESH anxiety
disease MESH fatigue
disease MESH infection
disease MESH brain fog
disease MESH headaches
disease MESH joint pain
drug DRUGBANK Methionine
disease MESH neuropathic pain
disease MESH autoimmune disease
drug DRUGBANK Papain
pathway REACTOME Digestion
drug DRUGBANK Immune Globulin Human
drug DRUGBANK Calcitonin gene-related peptide
disease MESH neuroinflammation
disease MESH cognitive symptoms
disease MESH Image
disease MESH mechanical allodynia

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