Washington University Study Links Alzheimer’s Protein Marker to CTE Diagnosis
Researchers detect elevated eMTBR-tau243 levels in CTE patients, offering a potential blood-based diagnostic breakthrough for the brain disorder.
POLICY WIRE — St. Louis, United States — A preliminary study suggests that measuring a specific toxic protein associated with Alzheimer’s disease could eventually help diagnose chronic traumatic encephalopathy, or CTE, in living patients. The discovery offers a potential pathway for identifying the brain condition, which has long defied confirmation until after death.
Currently, clinicians must rely on behavioral symptoms like memory loss and mood instability to suspect CTE, a disease linked to repeated head trauma and concussions. This diagnostic approach is complicated by overlapping symptoms common to other neurological disorders. Definitive diagnosis has traditionally required a post-mortem examination of brain tissue.
The breakthrough centers on tau, a protein that normally supports neuron function but becomes abnormal and tangles within nerve cells in Alzheimer’s patients. Scientists at Washington University in St. Louis were analyzing autopsy samples to track a specific tau fragment known as eMTBR-tau243 when they observed an anomaly in a patient with advanced CTE but no history of Alzheimer’s.
That patient displayed high levels of the biomarker despite records ruling out Alzheimer’s disease. Prompted by this unexpected finding, the research team expanded their investigation to a broader collection of autopsied tissues and blood samples derived from 11 individuals confirmed to have CTE.
Chihiro Sato, an assistant neurology professor at WashU and a coauthor of the study, noted that eMTBR-tau243 levels were significantly higher in CTE patients compared to healthy controls. However, Sato clarified that the biomarker did not reliably indicate early-stage CTE, limiting its immediate diagnostic scope.
Experts caution against over-interpreting the results. Dr. Rudolph Castellani, a neuropathologist at Northwestern University who was not involved in the research, described the findings as interesting but highly preliminary. He emphasized that much larger studies are required to confirm a genuine connection between the protein marker and the disease.
The complexity of the issue is compounded by the fact that abnormal tau appears in several brain conditions that frequently overlap in older adults. This convergence makes it difficult to isolate the protein’s specific role in CTE. Sato, who specializes in these tau-related disorders, echoed the need for extensive further research to validate the initial observations.
The findings were reported in the medical journal JAMA late Friday. The research was also presented at a scientific conference held in Japan. This publication marks a significant step in understanding the biological mechanisms underlying traumatic encephalopathy.
Reporting by Policy-Wire (PW)



