CaM Kinase II (CaMKII) is a critical enzyme involved in many essential brain functions, including neurotransmitter release, receptor activity, synaptic plasticity, learning, and memory. In the context of neuro-immune conditions, CaMKII serves as a functional marker that reflects how autoantibodies interact with neuronal cells.
This test measures the percentage increase in CaMKII activity when neuronal cells are exposed to a patient’s serum and compares it to a baseline reference. If autoantibodies in the blood bind to neuronal receptors or cell-surface molecules—such as dopamine receptors, tubulin, or lysogangliosides—they may stimulate or dysregulate CaMKII activity. Increased CaMKII activation suggests the immune system may be influencing intracellular signaling pathways that regulate mood, behavior, motor function, and cognition.
Elevated CaMKII activation has been observed in individuals with PANS (Pediatric Acute-Onset Neuropsychiatric Syndrome), PANDAS, Sydenham chorea, and other post-infectious or autoimmune neurological conditions. These conditions often follow infections such as strep, mycoplasma, or viral illnesses that can trigger an immune response affecting the brain.
CaMKII is a core component of the Autoimmune Brain Panel™, where it complements the four neuronal autoantibody titers (DRD1, DRD2L, anti-tubulin, anti-lysoganglioside GM1). While CaMKII elevation alone does not diagnose any disorder, it provides functional evidence that autoantibodies may be altering neuronal signaling. Interpreting CaMKII levels together with the other markers and clinical symptoms gives a clearer understanding of possible immune-mediated contributions to sudden-onset OCD, tics, anxiety, mood changes, movement abnormalities, regression, or behavioral shifts.
CaM Kinase II (CaMKII), % of Baseline
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