The role of apolipoprotein E episilon (<b>ɛ</b>)-4 allele on outcome following traumatic brain injury: A systematic review

Lawrence, David Wyndham; Comper, Paul; Hutchison, Michael; Sharma, Bhanu

doi:10.3109/02699052.2015.1005131

Cited by 72 publications

(58 citation statements)

References 118 publications

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“…27 Experimental data indicate that TBI in triple transgenic AD model mice causes accumulation and aggregation of Ab oligomers in the brain, which may contribute to developing AD later in life. 40 Genetic factors, such as presence of an ApoE4 allele 44 or neprilysin gene transfer (GT) repeat polymorphism 45 may potentially explain the bimodal distribution of Ab42 after TBI. Testing such a hypothesis will require a larger sample size, as the number of patients in our cohort was too small to allow adequately powered allelic association studies.…”

Section: Discussionmentioning

confidence: 99%

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Bogoslovsky

Wilson

Yao

et al. 2017

Journal of Neurotrauma

174

126

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Glial fibrillary acidic protein (GFAP), microtubule-associated protein tau, and amyloid b peptide (Ab42) have been proposed as diagnostic and prognostic biomarkers in traumatic brain injury (TBI). Single molecule array (Simoa) is a novel technology that employs highly sensitive immunoassays for accurate measurements of candidate biomarkers found at low concentration in biological fluids. Our objective was to trace the trajectory of tau, GFAP, and Ab42 levels in plasma from the acute through subacute stages after TBI, compared with controls. Samples from 34 TBI subjects enrolled in the Citicoline Brain Injury Treatment Trial (COBRIT) were studied. Injury severity was assessed by Glasgow Coma Scale (GCS) and admission CT. Glasgow Outcome Scale Extended (GOSE) was assessed 6 months after injury. Plasma was collected within 24 h (Day 0), and 30 and 90 days after the TBI. Plasma collected from 69 healthy volunteers was used for comparison. At every time point, increases were noted in plasma GFAP ( p < 0.0001 for all comparisons), tau ( p < 0.0001, p < 0.0001, and p = 0.0044, at Days 0, 30, and 90, respectively), and Ab42 ( p < 0.001, p < 0.0001, and p = 0.0203, respectively) in TBI cases compared with controls. The levels were maximal at Day 0 for GFAP and tau and at Day 30 for Ab42. Area under curve (AUC) analyses for Day 0 GFAP and tau were excellent for discrimination of complicated mild TBI (cmTBI) from controls (0.936 and 0.901, correspondingly). Discriminant component analysis (DCA) for all three biomarkers at Days 0 and 30 differentiated controls from cmTBI (91.1% and 89.7% correctly classified, at each time point). Duration of post-traumatic amnesia (PTA) correlated weakly with tau levels at 30 days (Spearman's r = 0.40; 95% CI 0.0003-0.60, p = 0.044). The Marshall CT Grade on admission correlated weakly with Day 30 tau levels (Spearman's r = 0.41; 95% CI 0.04-0.68, p = 0.027). Day 30 Ab42 correlated with GOSE (standardized b -0.486, p = 0.042). GFAP, tau and Ab42 were increased up to 90 days after TBI compared with controls. Total tau levels correlated with clinical and radiological variables of TBI severity. Plasma Ab42 correlated with clinical outcome. Combination of all three biomarkers at Days 0 and 30 can be used to differentiate controls from cmTBI populations, and may be useful as biomarkers of TBI in both acute and subacute phases.

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Section: Discussionmentioning

confidence: 99%

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Bogoslovsky

Wilson

Yao

et al. 2017

Journal of Neurotrauma

174

126

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“…The authors reported that moderate-to-severe TBI was associated with a higher likelihood for developing dementia in persons aged 55 years and older, whereas a single, mild TBI was associated with increased risk among those older than 64 years. In addition, a “synergistic” link between Apoe4 and a history of TBI is even less clear, as this literature too has been mixed, with approximately 50% of studies reporting an absence of an additive effect on increasing risk for developing dementia (Lawrence, Comper, Hutchison, & Sharma, 2015). More severe TBI may be an important factor (Lawrence et al, 2015), but some Apoe4 carriers could also possess the Apoe ε2 (Apoe2) allele (genotype ε2/ ε4), which has been implicated as protective against neuronal injury (Miller et al, 2010) and from AD (Corder et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, a “synergistic” link between Apoe4 and a history of TBI is even less clear, as this literature too has been mixed, with approximately 50% of studies reporting an absence of an additive effect on increasing risk for developing dementia (Lawrence, Comper, Hutchison, & Sharma, 2015). More severe TBI may be an important factor (Lawrence et al, 2015), but some Apoe4 carriers could also possess the Apoe ε2 (Apoe2) allele (genotype ε2/ ε4), which has been implicated as protective against neuronal injury (Miller et al, 2010) and from AD (Corder et al, 1994). It is possible that the presence of Apoe2 may offset Apoe4’s role in initiating and/or accelerating AD-like pathology, protecting against synergist mechanisms following TBI in some individuals, which could attenuate differences when comparing Apoe4 carriers to non-carriers.…”

Section: Discussionmentioning

confidence: 99%

Traumatic brain injury history is associated with earlier age of onset of Alzheimer disease

LoBue

Wadsworth

Wilmoth

et al. 2016

The Clinical Neuropsychologist

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Objective This study examined whether a history of traumatic brain injury (TBI) is associated with earlier onset of Alzheimer disease (AD), independent of apolipoprotein ε4 status (Apoe4) and gender. Method Participants with a clinical diagnosis of AD (n=7625) were obtained from the National Alzheimer’s Coordinating Center Uniform Data Set, and categorized based on self-reported lifetime TBI with loss of consciousness (LOC) (TBI+ vs TBI-) and presence of Apoe4. ANCOVAs, controlling for gender, race, and education were used to examine the association between history of TBI, presence of Apoe4, and an interaction of both risk factors on estimated age of AD onset. Results Estimated AD onset differed by TBI history and Apoe4 independently (p’s <.001). The TBI+ group had a mean age of onset 2.5 years earlier than the TBI- group. Likewise, Apoe4 carriers had a mean age of onset 2.3 years earlier than non-carriers. While the interaction was non-significant (p = .34), participants having both a history of TBI and Apoe4 had the earliest mean age of onset compared to those with a TBI history or Apoe4 alone (MDifference = 2.8 & 2.7 years, respectively). These results remained unchanged when stratified by gender. Conclusions History of self-reported TBI can be associated with an earlier onset of AD-related cognitive decline, regardless of Apoe4 status and gender. TBI may be related to an underlying neurodegenerative process in AD, but the implications of age at time of injury, severity, and repetitive injuries remain unclear.

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“…ApoE ε3 has a neuroprotective effect that protects against neurodegeneration and cognitive decline, while ApoE ε4 has the opposite effect, resulting in an overall negative influence on several neuroplastic processes. 66, 67 The ApoE ε4 allele is a risk factor for Alzheimer’s disease 68 and is related to poorer outcome after traumatic brain injury 69 and stroke. 70–72 …”

Section: Genetic Polymorphisms Neuroplasticity and Motor Learningmentioning

confidence: 99%

Genetic Variation and Neuroplasticity: Role in Rehabilitation After Stroke

Stewart

Cramer

2017

Journal of Neurologic Physical Therapy

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Background and Purpose In many neurologic diagnoses significant inter-individual variability exits in the outcomes of rehabilitation. One factor that may impact response to rehabilitation interventions is genetic variation. Genetic variation refers to the presence of differences in the DNA sequence among individuals in a population. Genetic polymorphisms are variations that occur relatively commonly and, while not disease-causing, can impact the function of biological systems. The purpose of this article is to describe genetic polymorphisms that may impact neuroplasticity, motor learning, and recovery after stroke. Summary of Key Points Genetic polymorphisms for brain-derived neurotrophic factor (BDNF), dopamine, and apolipoprotein E have been shown to impact neuroplasticity and motor learning. Rehabilitation interventions that rely on the molecular and cellular pathways of these factors may be impacted by the presence of the polymorphism. For example, it has been hypothesized that individuals with the BDNF polymorphism may show a decreased response to neuroplasticity-based interventions, decreased rate of learning, and overall less recovery after stroke. However, research to date has been limited and additional work is needed to fully understand the role of genetic variation in learning and recovery. Recommendations for Clinical Practice Genetic polymorphisms should be considered as possible predictors or covariates in studies that investigate neuroplasticity, motor learning, or motor recovery after stroke. Future predictive models of stroke recovery will likely include a combination of genetic factors and other traditional factors (e.g. age, lesion type, corticospinal tract integrity) to determine an individual’s expected response to a specific rehabilitation intervention.

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The role of apolipoprotein E episilon (ɛ)-4 allele on outcome following traumatic brain injury: A systematic review

Cited by 72 publications

References 118 publications

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Increases of Plasma Levels of Glial Fibrillary Acidic Protein, Tau, and Amyloid β up to 90 Days after Traumatic Brain Injury

Traumatic brain injury history is associated with earlier age of onset of Alzheimer disease

Genetic Variation and Neuroplasticity: Role in Rehabilitation After Stroke

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