Apolipoprotein E polymorphism and outcome after closed traumatic brain injury: influence of ethnic and regional differences

Nathoo, Narendra; Chetty, Runjan; Dellen, James R. van; Connolly, Catherine; Naidoo, Richard

doi:10.3171/jns.2003.98.2.0302

Cited by 63 publications

(51 citation statements)

References 30 publications

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“…Nathoo et al. noted that APOE‐ ε 4 carriers show a greater propensity for developing age‐related cognitive impairment, a decrease in the synapse‐neuron ratio, and an increased susceptibility to exogenous neurotoxins and hippocampal atrophy independent of head trauma (Nathoo, Chetry, van Dellen, Connolly, & Naidoo, 2003). …”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

“…The relationship between race and CVLT‐II has been previously described (Delis et al., 2000; Nathoo et al., 2003). In our study, race was associated with CVLT performance after injury.…”

Section: Discussionmentioning

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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“…Nevertheless, several groups of authors have expressed doubt about the correlation. 42,49,56 In a detailed neuropsychological assessment of 90 adult patients with mild and moderate TBI at 6-month followup, investigators found no effect of APOE e4 allele poor outcome. 9 Some studies have even revealed that e4 carriers performed better on measures of attention, executive functioning, and episodic memory encoding than do noncarriers.…”

Section: Apoe and Head Injurymentioning

confidence: 99%

Role of apolipoprotein E polymorphism as a prognostic marker in traumatic brain injury and neurodegenerative disease: a critical review

Maiti¹,

Konar²,

Bir³

et al. 2015

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OBJECT The difference in course and outcome of several neurodegenerative conditions and traumatic injuries of the nervous system points toward a possible role of genetic and environmental factors as prognostic markers. Apolipoprotein E (Apo-E), a key player in lipid metabolism, is recognized as one of the most powerful genetic risk factors for dementia and other neurodegenerative diseases. In this article, the current understanding of APOE polymorphism in various neurological disorders is discussed. METHODS The English literature was searched for various studies describing the role of APOE polymorphism as a prognostic marker in neurodegenerative diseases and traumatic brain injury. The wide ethnic distribution of APOE polymorphism was discussed, and the recent meta-analyses of role of APOE polymorphism in multiple diseases were analyzed and summarized in tabular form. RESULTS Results from the review of literature revealed that the distribution of APOE is varied in different ethnic populations. APOE polymorphism plays a significant role in pathogenesis of neurodegeneration, particularly in Alzheimer’s disease. APOE ε4 is considered a marker for poor prognosis in various diseases, but APOE ε2 rather than APOE ε4 has been associated with cerebral amyloid angiopathy-related bleeding and sporadic Parkinson’s disease. The role of APOE polymorphism in various neurological diseases has not been conclusively elucidated. CONCLUSIONS Apo-E is a biomarker for various neurological and systemic diseases. Therefore, while analyzing the role of APOE polymorphism in neurological diseases, the interpretation should be done after adjusting all the confounding factors. A continuous quest to look for associations with various neurological diseases and wide knowledge of available literature are required to improve the understanding of the role of APOE polymorphism in these conditions and identify potential therapeutic targets.

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“…2,12,15,17,25,40,69,87,98,130,131,135 In a recent meta-analysis of 14 cohort studies (of 23 relevant studies identified from the literature) and 2427 participants, it was found that the ApoE4 allele increases the risk of poor clinical outcome, which was evaluated 6 months after the injury. 139 The ApoE polymorphism was also tested in patients who had suffered TBI in relation to several other neuropathological, laboratory, or imaging intermediate phenotypes, such as Aβ deposition, 100 hippocampal volume and brain atrophy, 48 cerebral blood flow, 59 presence of brain lesions, 41 In addition to the aforementioned coding sequence polymorphisms, the ApoE gene is also polymorphic in the regulatory region.…”

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confidence: 99%

Genetic association studies in patients with traumatic brain injury

Dardiotis

Fountas²,

Dardioti

et al. 2010

FOC

110

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Traumatic brain injury (TBI) constitutes a major cause of mortality and disability worldwide, especially among young individuals. It is estimated that despite all the recent advances in the management of TBI, approximately half of the patients suffering head injuries still have unfavorable outcomes, which represents a substantial health care, social, and economic burden to societies. Considerable variability exists in the clinical outcome after TBI, which is only partially explained by known factors. Accumulating evidence has implicated various genetic elements in the pathophysiology of brain trauma. The extent of brain injury after TBI seems to be modulated to some degree by genetic variants. The authors' current review focuses on the up-to-date state of knowledge regarding genetic association studies in patients sustaining TBI, with particular emphasis on the mechanisms underlying the implication of genes in the pathophysiology of TBI.

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Apolipoprotein E polymorphism and outcome after closed traumatic brain injury: influence of ethnic and regional differences

Cited by 63 publications

References 30 publications

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

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

Role of apolipoprotein E polymorphism as a prognostic marker in traumatic brain injury and neurodegenerative disease: a critical review

Genetic association studies in patients with traumatic brain injury

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