TY - JOUR
T1 - Apolipoprotein E epsilon 4 (APOE-ε4) genotype is associated with decreased 6-month verbal memory performance after mild traumatic brain injury
AU - the TRACK-TBI Investigators
AU - Yue, John K.
AU - Robinson, Caitlin K.
AU - Burke, John F.
AU - Winkler, Ethan A.
AU - Deng, Hansen
AU - Cnossen, Maryse C.
AU - Lingsma, Hester F.
AU - Ferguson, Adam R.
AU - McAllister, Thomas W.
AU - Rosand, Jonathan
AU - Burchard, Esteban G.
AU - Sorani, Marco D.
AU - Sharma, Sourabh
AU - Nielson, Jessica L.
AU - Satris, Gabriela G.
AU - Talbott, Jason F.
AU - Tarapore, Phiroz E.
AU - Korley, Frederick K.
AU - Wang, Kevin K.W.
AU - Yuh, Esther L.
AU - Mukherjee, Pratik
AU - Diaz-Arrastia, Ramon
AU - Valadka, Alex B.
AU - Okonkwo, David O.
AU - Manley, Geoffrey T.
N1 - Publisher Copyright:
© 2017 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.
PY - 2017/9
Y1 - 2017/9
N2 - Introduction: The apolipoprotein E (APOE) ε4 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 APOE genotyping results were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study. Cohorts determined by APOE-ε4(+/−) 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 (APOE-ε4(−)=79; APOE-ε4(+)=35), ApoE-ε4(+) was associated with long-delay verbal memory deficits (LDFR: B = −1.17 points, 95% CI [−2.33, −0.01], p =.049; LDCR: B = −1.58 [−2.63, −0.52], p =.004), and a marginal decrease on SDCR (B = −1.02 [−2.05, 0.00], p =.050). CT pathology was the strongest predictor of decreased verbal memory (IRT: B = −8.49, SDFR: B = −2.50, SDCR: B = −1.85, LDFR: B = −2.61, LDCR: B = −2.60; p <.001). Seizure history was associated with decreased short-term memory (SDFR: B = −1.32, p =.037; SDCR: B = −1.44, p =.038). Conclusion: The APOE-ε4 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.
AB - Introduction: The apolipoprotein E (APOE) ε4 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 APOE genotyping results were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Pilot (TRACK-TBI Pilot) study. Cohorts determined by APOE-ε4(+/−) 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 (APOE-ε4(−)=79; APOE-ε4(+)=35), ApoE-ε4(+) was associated with long-delay verbal memory deficits (LDFR: B = −1.17 points, 95% CI [−2.33, −0.01], p =.049; LDCR: B = −1.58 [−2.63, −0.52], p =.004), and a marginal decrease on SDCR (B = −1.02 [−2.05, 0.00], p =.050). CT pathology was the strongest predictor of decreased verbal memory (IRT: B = −8.49, SDFR: B = −2.50, SDCR: B = −1.85, LDFR: B = −2.61, LDCR: B = −2.60; p <.001). Seizure history was associated with decreased short-term memory (SDFR: B = −1.32, p =.037; SDCR: B = −1.44, p =.038). Conclusion: The APOE-ε4 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.
KW - apolipoprotein E
KW - genetic factors
KW - human studies
KW - outcome measures
KW - traumatic brain injury
KW - verbal memory
UR - http://www.scopus.com/inward/record.url?scp=85029804514&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85029804514&partnerID=8YFLogxK
U2 - 10.1002/brb3.791
DO - 10.1002/brb3.791
M3 - Article
C2 - 28948085
AN - SCOPUS:85029804514
SN - 2157-9032
VL - 7
JO - Brain and Behavior
JF - Brain and Behavior
IS - 9
M1 - e00791
ER -