Does Apolipoprotein e4 Status Moderate the Association of Family Environment with Long-Term Child Functioning following Early Moderate to Severe Traumatic Brain Injury? A Preliminary Study

Treble‐Barna, Amery; Zang, Huaiyu; Zhang, Nanhua; Martin, Lisa J.; Yeates, Keith Owen; Taylor, H. Gerry; Wade, Shari L.; Kurowski, Brad G.

doi:10.1017/s1355617716000631

Cited by 10 publications

(7 citation statements)

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“…There have been various studies that focused on neurological disorders during childhood and adolescence that attempted to identify possible meaningful correlations between manifestation and progression of a disease, or its variable phenotypic characterization, and the APOE genotype. Initial findings by Treble-Barna et al [152] suggest an APOE -environmental interaction in terms of long-term outcomes in children with a history of traumatic brain injury (TBI). This possible gene-environmental interaction has been further suggested by Kassam et al [153] based on meta-analytic results showing that APOE 4 is undoubtedly associated with a worse prognosis after a TBI in both children and young adults and that this effect might be due to mechanisms quite different from those linked to neurodegeneration during aging.…”

Section: Apoe Polymorphism In Normal and Pathologic Conditions Of Thementioning

confidence: 99%

Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan

Iacono

Feltis

2019

Aging

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The central nervous system (CNS) is the cellular substrate for the integration of complex, dynamic, constant, and simultaneous interactions among endogenous and exogenous stimuli across the entire human lifespan. Numerous studies on aging-related brain diseases show that some genes identified as risk factors for some of the most common neurodegenerative diseases - such as the allele 4 of APOE gene (APOE4) for Alzheimer’s disease (AD) - have a much earlier neuro-anatomical and neuro-physiological impact. The impact of APOE polymorphism appears in fact to start as early as youth and early-adult life. Intriguingly, though, those same genes associated with aging-related brain diseases seem to influence different aspects of the brain functioning much earlier actually, that is, even from the neonatal periods and earlier. The APOE4, an allele classically associated with later-life neurodegenerative disorders as AD, seems in fact to exert a series of very early effects on phenomena of neuroplasticity and synaptogenesis that begin from the earliest periods of life such as the fetal ones.We reviewed some of the findings supporting the hypothesis that APOE polymorphism is an early modifier of various neurobiological aspects across the entire human lifespan - from the in-utero to the centenarian life - during both normal and pathological conditions of the brain.

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Section: Apoe Polymorphism In Normal and Pathologic Conditions Of Thementioning

confidence: 99%

Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan

Iacono

Feltis

2019

Aging

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“…A growing body of evidence suggests that an individual's genetic makeup may also affect recovery. While most current pediatric research on genetics in TBI has focused on the apolipoprotein E (ApoE) gene 5,18,19 and catechol-O-methyltransferase (COMT), 20 research from the adult literature suggests that genes related to preinjury cognitive capacity and reserve also may be associated with EF following TBI. 21 Much of the current research has focused on genes involved in the dopaminergic and serotonergic pathways, which are pathways often implicated in post-TBI cognitive and social impairments.…”

Section: Introductionmentioning

confidence: 99%

The Moderating Effect of the Ankyrin Repeat and Kinase Domain Containing One Gene on the Association of Family Environment with Longitudinal Executive Function following Traumatic Brain Injury in Early Childhood: A Preliminary Study

Smith-Paine

Wade

Treble‐Barna

et al. 2018

Journal of Neurotrauma

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This study examined whether the ankyrin repeat and kinase domain containing 1 gene (ANKK1) C/T single-nucleotide polymorphism (SNP) rs1800497 moderated the association of family environment with long-term executive function (EF) following traumatic injury in early childhood. Caregivers of children with traumatic brain injury (TBI) and children with orthopedic injury completed the Behavior Rating Inventory of Executive Function (BRIEF) at post-injury visits. DNA was collected to identify the rs1800497 genotype in the ANKK1 gene. General linear models examined gene-environment interactions as moderators of the effects of TBI on EF at two times post-injury (12 months and 7 years). At 12 months post-injury, analyses revealed a significant three-way interaction of genotype with level of permissive parenting and injury type. Post hoc analyses showed genetic effects were more pronounced for children with TBI from more positive family environments, such that children with TBI who were carriers of the risk allele (T-allele) had significantly poorer EF compared with non-carriers only when they were from more advantaged environments. At 7 years post-injury, analyses revealed a significant two-way interaction of genotype with level of authoritarian parenting. Post hoc analyses found that carriers of the risk allele had significantly poorer EF compared with non-carriers only when they were from more advantaged environments. These results suggest a gene-environment interaction involving the ANKK1 gene as a predictor of EF in a pediatric injury population. The findings highlight the importance of considering environmental influences in future genetic studies on recovery following TBI and other traumatic injuries in childhood.

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“…Conversely in children, Moran et al report that the APOE-ε4 allele has little impact on neurocognitive measures following TBI, although ε4-carriers were associated with a more negative early response to injury (Moran et al, 2009), which mirrors the adult literature (Friedman et al, 1999;Jiang et al, 2006). Interestingly, pediatric ε4 carriers sustaining moderate to severe TBI showed poorer adaptive functioning in the context of positive parenting, whereas non-ε4-carriers displayed worse detriments in the context of less optimal parenting (Treble- Barna et al, 2016). These studies further highlight the pleiotropic association between APOE-ε4 and neurobehavioral outcomes after TBI, and underscore the need to elucidate its relationship with outcome subdomains after different types of TBI.…”

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confidence: 99%

Apolipoprotein E epsilon 4 (APOE‐ε4) genotype is associated with decreased 6‐month verbal memory performance after mild traumatic brain injury

et al. 2017

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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.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).ResultsIn 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).ConclusionThe 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.

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Does Apolipoprotein e4 Status Moderate the Association of Family Environment with Long-Term Child Functioning following Early Moderate to Severe Traumatic Brain Injury? A Preliminary Study

Cited by 10 publications

References 28 publications

Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan

Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan

The Moderating Effect of the Ankyrin Repeat and Kinase Domain Containing One Gene on the Association of Family Environment with Longitudinal Executive Function following Traumatic Brain Injury in Early Childhood: A Preliminary Study

Apolipoprotein E epsilon 4 (APOE‐ε4) genotype is associated with decreased 6‐month verbal memory performance after mild traumatic brain injury

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