Apolipoprotein E epsilon 4 (APOEâ ε4) genotype is associated with decreased 6â month verbal memory performance after mild traumatic brain injury
Yue, John K.; Robinson, Caitlin K.; Burke, John F.; Winkler, Ethan A.; Deng, Hansen; Cnossen, Maryse C.; Lingsma, Hester F.; Ferguson, Adam R.; McAllister, Thomas W.; Rosand, Jonathan; Burchard, Esteban G.; Sorani, Marco D.; Sharma, Sourabh; Nielson, Jessica L.; Satris, Gabriela G.; Talbott, Jason F.; Tarapore, Phiroz E.; Korley, Frederick K.; Wang, Kevin K.W.; Yuh, Esther L.; Mukherjee, Pratik; Diaz‐arrastia, Ramon; Valadka, Alex B.; Okonkwo, David O.; Manley, Geoffrey T.
2017-09
Citation
Yue, John K.; Robinson, Caitlin K.; Burke, John F.; Winkler, Ethan A.; Deng, Hansen; Cnossen, Maryse C.; Lingsma, Hester F.; Ferguson, Adam R.; McAllister, Thomas W.; Rosand, Jonathan; Burchard, Esteban G.; Sorani, Marco D.; Sharma, Sourabh; Nielson, Jessica L.; Satris, Gabriela G.; Talbott, Jason F.; Tarapore, Phiroz E.; Korley, Frederick K.; Wang, Kevin K.W.; Yuh, Esther L.; Mukherjee, Pratik; Diaz‐arrastia, Ramon ; Valadka, Alex B.; Okonkwo, David O.; Manley, Geoffrey T. (2017). "Apolipoprotein E epsilon 4 (APOEâ ε4) genotype is associated with decreased 6â month verbal memory performance after mild traumatic brain injury." Brain and Behavior 7(9): n/a-n/a.
Abstract
IntroductionThe apolipoprotein E (APOE) ε4 allele associates with memory impairment in neurodegenerative diseases. Its association with memory after mild traumatic brain injury (mTBI) is unclear.MethodsmTBI patients (Glasgow Coma Scale score 13â 15, no neurosurgical intervention, extracranial Abbreviated Injury Scale score â ¤1) aged â ¥18 years with APOE genotyping results were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACKâ TBI Pilot) study. Cohorts determined by APOEâ ε4(+/â ) were assessed for associations with 6â month verbal memory, measured by California Verbal Learning Test, Second Edition (CVLTâ II) subscales: Immediate Recall Trials 1â 5 (IRT), Shortâ Delay Free Recall (SDFR), Shortâ Delay Cued Recall (SDCR), Longâ Delay Free Recall (LDFR), and Longâ 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).ResultsIn 114 mTBI patients (APOEâ ε4(â )=79; APOEâ ε4(+)=35), ApoEâ ε4(+) was associated with longâ delay verbal memory deficits (LDFR: B = â 1.17 points, 95% CI [â 2.33, â 0.01], p = .049; LDCR: B = â 1.58 [â 2.63, â 0.52], p = .004), and a marginal decrease on SDCR (B = â 1.02 [â 2.05, 0.00], p = .050). CT pathology was the strongest predictor of decreased verbal memory (IRT: B = â 8.49, SDFR: B = â 2.50, SDCR: B = â 1.85, LDFR: B = â 2.61, LDCR: B = â 2.60; p < .001). Seizure history was associated with decreased shortâ term memory (SDFR: B = â 1.32, p = .037; SDCR: B = â 1.44, p = .038).ConclusionThe APOEâ ε4 allele may confer an increased risk of impairment of 6â 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.In 114 adult mild traumatic brain injury (mTBI) patients without polytrauma, APOEâ ε4(+) status was associated with decreased 6â month verbal memory performance on longâ delay free and cued recall subtests of the California Verbal Learning Test, Second Edition after controlling for demographic and clinical variables. The APOEâ ε4 allele may confer an increased risk of longâ term verbal memory impairment following mTBI, with implications for heightened surveillance and targeted therapies.Publisher
Psychological Corporation Wiley Periodicals, Inc.
ISSN
2162-3279 2162-3279
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