ε genotype is associated with decreased 6-month verbal memory performance after mild traumatic brain injury.

Introduction: The apolipoprotein E () ε allele associates with memory impairment in neurodegenerative diseases. Its association with memory after mild traumatic brain injury (mTBI) is unclear.

Methods: mTBI patients (Glasgow Coma Scale score 13-15, no neurosurgical intervention, extracranial Abbreviated Injury Scale score ≤1) aged ≥18 years with genotyping results were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study. Cohorts determined by ε were assessed for associations with 6-month verbal memory, measured by California Verbal Learning Test, Second Edition (CVLT-II) subscales: Immediate Recall Trials 1-5 (IRT), Short-Delay Free Recall (SDFR), Short-Delay Cued Recall (SDCR), Long-Delay Free Recall (LDFR), and Long-Delay Cued Recall (LDCR). Multivariable regression controlled for demographic factors, seizure history, loss of consciousness, posttraumatic amnesia, and acute intracranial pathology on computed tomography (CT).

Results: In 114 mTBI patients (ε=79; ε=35), ε was associated with long-delay verbal memory deficits (LDFR: =-1.17 points, 95% CI [-2.33, -0.01], =.049; LDCR: =-1.58 [-2.63, -0.52], =.004), and a marginal decrease on SDCR (=-1.02 [-2.05, 0.00], =.050). CT pathology was the strongest predictor of decreased verbal memory (IRT: =-8.49, SDFR: =-2.50, SDCR: -1.85, LDFR: -2.61, LDCR: -2.60; <.001). Seizure history was associated with decreased short-term memory (SDFR: -1.32, =.037; SDCR: -1.44, =.038).

Conclusion: The ε allele may confer an increased risk of impairment of 6-month verbal memory for patients suffering mTBI, with implications for heightened surveillance and targeted therapies. Acute intracranial pathology remains the driver of decreased verbal memory performance at 6 months after mTBI.