Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {*Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Calcagnile, O; Anell, A; Unden, J
The addition of S100B to guidelines for management of mild head injury is potentially cost saving Journal Article
In: BMC Neurology, vol. 16, no. 1, pp. 200, 2016.
Abstract | BibTeX | Tags: *Brain Concussion/bl [Blood], *Brain Concussion/ec [Economics], *Cost Savings, *Practice Guidelines as Topic, *S100 Calcium Binding Protein beta Subunit/bl [Blo, 0 (Biomarkers), 0 (S100 Calcium Binding Protein beta Subunit), 80 and over, Adolescent, adult, aged, Biomarkers/bl [Blood], Female, Humans, Male, middle aged, SWEDEN, Young Adult
@article{Calcagnile2016,
title = {The addition of S100B to guidelines for management of mild head injury is potentially cost saving},
author = {Calcagnile, O and Anell, A and Unden, J},
year = {2016},
date = {2016-01-01},
journal = {BMC Neurology},
volume = {16},
number = {1},
pages = {200},
abstract = {BACKGROUND: Mild traumatic brain injury (TBI) is associated with substantial costs due to over-triage of patients to computed tomography (CT) scanning, despite validated decision rules. Serum biomarker S100B has shown promise for safely omitting CT scans but the economic impact from clinical use has never been reported. In 2007, S100B was adapted into the existing Scandinavian management guidelines in Halmstad, Sweden, in an attempt to reduce CT scans and save costs. METHODS: Consecutive adult patients with mild TBI (GCS 14-15, loss of consciousness and/or amnesia), managed with the aid of S100B, were prospectively included in this study. Patients were followed up after 3 months with a standardized questionnaire. Theoretical and actual cost differences were calculated. RESULTS: Seven hundred twenty-six patients were included and 29 (4.7 %) showed traumatic abnormalities on CT. No further significant intracranial complications were discovered on follow-up. Two hundred twenty-nine patients (27 %) had normal S100B levels and 497 patients (73 %) showed elevated S100B levels. Over-triage occurred in 73 patients (32 %) and under-triage occurred in 39 patients (7 %). No significant intracranial complications were missed. The introduction of S100B could save 71 per patient if guidelines were strictly followed. As compliance to the guidelines was not perfect, the actual cost saving was 39 per patient. CONCLUSION: Adding S100B to existing guidelines for mild TBI seems to reduce CT usage and costs, especially if guideline compliance could be increased.},
keywords = {*Brain Concussion/bl [Blood], *Brain Concussion/ec [Economics], *Cost Savings, *Practice Guidelines as Topic, *S100 Calcium Binding Protein beta Subunit/bl [Blo, 0 (Biomarkers), 0 (S100 Calcium Binding Protein beta Subunit), 80 and over, Adolescent, adult, aged, Biomarkers/bl [Blood], Female, Humans, Male, middle aged, SWEDEN, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}
Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]},
pubstate = {published},
tppubtype = {article}
}
Chetelat, G; Eustache, F; Viader, F; De La Sayette, V; Pelerin, A; Mezenge, F; Hannequin, D; Dupuy, B; Baron, J C; Desgranges, B
FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment Journal Article
In: Neurocase, vol. 11, no. 1, pp. 14–25, 2005.
Abstract | BibTeX | Tags: *Cognition Disorders/dg [Diagnostic Imaging], *Fluorodeoxyglucose F18, *Neuropsychological Tests, *Positron-Emission Tomography, 0Z5B2CJX4D (Fluorodeoxyglucose F18), 80 and over, aged, ANALYSIS of variance, Brain Concussion/dg [Diagnostic Imaging], Brain Concussion/pa [Pathology], BRAIN mapping, Cognition Disorders/di [Diagnosis], Dementia/dg [Diagnostic Imaging], Dementia/di [Diagnosis], Dementia/pp [Physiopathology], Female, Follow-Up Studies, Humans, Male, Memory/ph [Physiology], Mental Status Schedule, middle aged, Predictive Value of Tests, Regression (Psychology), Reproducibility of Results, Time Factors
@article{Chetelat2005,
title = {FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment},
author = {Chetelat, G and Eustache, F and Viader, F and {De La Sayette}, V and Pelerin, A and Mezenge, F and Hannequin, D and Dupuy, B and Baron, J C and Desgranges, B},
year = {2005},
date = {2005-01-01},
journal = {Neurocase},
volume = {11},
number = {1},
pages = {14--25},
abstract = {The accurate prediction, at a pre-dementia stage of Alzheimer's disease (AD), of the subsequent clinical evolution of patients would be a major breakthrough from both therapeutic and research standpoints. Amnestic mild cognitive impairment (MCI) is presently the most common reference to address the pre-dementia stage of AD. However, previous longitudinal studies on patients with MCI assessing neuropsychological and PET markers of future conversion to AD are sparse and yield discrepant findings, while a comprehensive comparison of the relative accuracy of these two categories of measure is still lacking. In the present study, we assessed the global cognitive decline as measured by the Mattis scale in 18 patients with amnestic MCI over an 18-month follow-up period, studying which subtest of this scale showed significant deterioration over time. Using baseline measurements from neuropsychological evaluation of memory and PET, we then assessed significant markers of global cognitive change, that is, percent annual change in the Mattis scale total score, and searched for the best predictor of this global cognitive decline. Altogether, our results revealed significant decline over the 18-month follow-up period in the total score and the verbal initiation and memory-recall subscores of the Mattis scale. The percent annual change in the total Mattis score significantly correlated with age and baseline performances in delayed episodic memory recall as well as semantic autobiographical and category word fluencies. Regarding functional imaging, significant correlations were also found with baseline PET values in the right temporo-parietal and medial frontal areas. Age and right temporo-parietal PET values were the most significant predictors of subsequent global cognitive decline, and the only ones to survive stepwise regression analyses. Our findings are consistent with previous works showing predominant delayed recall and semantic memory impairment at a pre-dementia stage of AD, as well as early metabolic defects in the temporo-parietal associative cortex. However, they suggest that only the latter predictor is specifically and accurately associated with subsequent cognitive decline in patients with MCI within 18 months of first assessment.},
keywords = {*Cognition Disorders/dg [Diagnostic Imaging], *Fluorodeoxyglucose F18, *Neuropsychological Tests, *Positron-Emission Tomography, 0Z5B2CJX4D (Fluorodeoxyglucose F18), 80 and over, aged, ANALYSIS of variance, Brain Concussion/dg [Diagnostic Imaging], Brain Concussion/pa [Pathology], BRAIN mapping, Cognition Disorders/di [Diagnosis], Dementia/dg [Diagnostic Imaging], Dementia/di [Diagnosis], Dementia/pp [Physiopathology], Female, Follow-Up Studies, Humans, Male, Memory/ph [Physiology], Mental Status Schedule, middle aged, Predictive Value of Tests, Regression (Psychology), Reproducibility of Results, Time Factors},
pubstate = {published},
tppubtype = {article}
}
Bigler, E D; Rosa, L; Schultz, F; Hall, S; Harris, J
Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013] Journal Article
In: Journal of Clinical Psychology, vol. 45, no. 2, pp. 277–280, 1989.
Abstract | BibTeX | Tags: *Alzheimer Disease/px [Psychology], *Brain Concussion/px [Psychology], *Form Perception, *MEMORY, *Mental Recall, *Neurocognitive Disorders/px [Psychology], *Neuropsychological Tests, *Pattern Recognition, *Verbal Learning, 80 and over, adult, aged, attention, Female, Humans, Male, middle aged, Psychometrics, SPEECH perception, Visual
@article{Bigler1989,
title = {Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013]},
author = {Bigler, E D and Rosa, L and Schultz, F and Hall, S and Harris, J},
year = {1989},
date = {1989-01-01},
journal = {Journal of Clinical Psychology},
volume = {45},
number = {2},
pages = {277--280},
abstract = {Performance on the Rey-Auditory Verbal Learning (R-AVL) and Rey-Osterrieth Complex Figure Design (R-O CFD) tests was examined in patients (N = 94) with dementia of the Alzheimer's type (DAT) and closed head injury (CHI). On the R-AVL, DAT patients demonstrated considerably greater impairment than CHI patients, along with a flat learning/retention curve that showed negligible improvement with repeated trials, recency effects only, and an excessive number of word intrusions (confabulation) on the recognition trial. CHI patients demonstrated both a recency and primacy effect along with improvement over repeated trials (positive slope learning curve). Both groups demonstrated impairment R-O CFD recall; the DAT group again displayed substantially greater copying and recall deficits. Clinical guidelines are given for the use of the R-AVL and R-O CFD for these two patient populations.},
keywords = {*Alzheimer Disease/px [Psychology], *Brain Concussion/px [Psychology], *Form Perception, *MEMORY, *Mental Recall, *Neurocognitive Disorders/px [Psychology], *Neuropsychological Tests, *Pattern Recognition, *Verbal Learning, 80 and over, adult, aged, attention, Female, Humans, Male, middle aged, Psychometrics, SPEECH perception, Visual},
pubstate = {published},
tppubtype = {article}
}
Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Calcagnile, O; Anell, A; Unden, J
The addition of S100B to guidelines for management of mild head injury is potentially cost saving Journal Article
In: BMC Neurology, vol. 16, no. 1, pp. 200, 2016.
@article{Calcagnile2016,
title = {The addition of S100B to guidelines for management of mild head injury is potentially cost saving},
author = {Calcagnile, O and Anell, A and Unden, J},
year = {2016},
date = {2016-01-01},
journal = {BMC Neurology},
volume = {16},
number = {1},
pages = {200},
abstract = {BACKGROUND: Mild traumatic brain injury (TBI) is associated with substantial costs due to over-triage of patients to computed tomography (CT) scanning, despite validated decision rules. Serum biomarker S100B has shown promise for safely omitting CT scans but the economic impact from clinical use has never been reported. In 2007, S100B was adapted into the existing Scandinavian management guidelines in Halmstad, Sweden, in an attempt to reduce CT scans and save costs. METHODS: Consecutive adult patients with mild TBI (GCS 14-15, loss of consciousness and/or amnesia), managed with the aid of S100B, were prospectively included in this study. Patients were followed up after 3 months with a standardized questionnaire. Theoretical and actual cost differences were calculated. RESULTS: Seven hundred twenty-six patients were included and 29 (4.7 %) showed traumatic abnormalities on CT. No further significant intracranial complications were discovered on follow-up. Two hundred twenty-nine patients (27 %) had normal S100B levels and 497 patients (73 %) showed elevated S100B levels. Over-triage occurred in 73 patients (32 %) and under-triage occurred in 39 patients (7 %). No significant intracranial complications were missed. The introduction of S100B could save 71 per patient if guidelines were strictly followed. As compliance to the guidelines was not perfect, the actual cost saving was 39 per patient. CONCLUSION: Adding S100B to existing guidelines for mild TBI seems to reduce CT usage and costs, especially if guideline compliance could be increased.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Chetelat, G; Eustache, F; Viader, F; De La Sayette, V; Pelerin, A; Mezenge, F; Hannequin, D; Dupuy, B; Baron, J C; Desgranges, B
FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment Journal Article
In: Neurocase, vol. 11, no. 1, pp. 14–25, 2005.
@article{Chetelat2005,
title = {FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment},
author = {Chetelat, G and Eustache, F and Viader, F and {De La Sayette}, V and Pelerin, A and Mezenge, F and Hannequin, D and Dupuy, B and Baron, J C and Desgranges, B},
year = {2005},
date = {2005-01-01},
journal = {Neurocase},
volume = {11},
number = {1},
pages = {14--25},
abstract = {The accurate prediction, at a pre-dementia stage of Alzheimer's disease (AD), of the subsequent clinical evolution of patients would be a major breakthrough from both therapeutic and research standpoints. Amnestic mild cognitive impairment (MCI) is presently the most common reference to address the pre-dementia stage of AD. However, previous longitudinal studies on patients with MCI assessing neuropsychological and PET markers of future conversion to AD are sparse and yield discrepant findings, while a comprehensive comparison of the relative accuracy of these two categories of measure is still lacking. In the present study, we assessed the global cognitive decline as measured by the Mattis scale in 18 patients with amnestic MCI over an 18-month follow-up period, studying which subtest of this scale showed significant deterioration over time. Using baseline measurements from neuropsychological evaluation of memory and PET, we then assessed significant markers of global cognitive change, that is, percent annual change in the Mattis scale total score, and searched for the best predictor of this global cognitive decline. Altogether, our results revealed significant decline over the 18-month follow-up period in the total score and the verbal initiation and memory-recall subscores of the Mattis scale. The percent annual change in the total Mattis score significantly correlated with age and baseline performances in delayed episodic memory recall as well as semantic autobiographical and category word fluencies. Regarding functional imaging, significant correlations were also found with baseline PET values in the right temporo-parietal and medial frontal areas. Age and right temporo-parietal PET values were the most significant predictors of subsequent global cognitive decline, and the only ones to survive stepwise regression analyses. Our findings are consistent with previous works showing predominant delayed recall and semantic memory impairment at a pre-dementia stage of AD, as well as early metabolic defects in the temporo-parietal associative cortex. However, they suggest that only the latter predictor is specifically and accurately associated with subsequent cognitive decline in patients with MCI within 18 months of first assessment.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Bigler, E D; Rosa, L; Schultz, F; Hall, S; Harris, J
Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013] Journal Article
In: Journal of Clinical Psychology, vol. 45, no. 2, pp. 277–280, 1989.
@article{Bigler1989,
title = {Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013]},
author = {Bigler, E D and Rosa, L and Schultz, F and Hall, S and Harris, J},
year = {1989},
date = {1989-01-01},
journal = {Journal of Clinical Psychology},
volume = {45},
number = {2},
pages = {277--280},
abstract = {Performance on the Rey-Auditory Verbal Learning (R-AVL) and Rey-Osterrieth Complex Figure Design (R-O CFD) tests was examined in patients (N = 94) with dementia of the Alzheimer's type (DAT) and closed head injury (CHI). On the R-AVL, DAT patients demonstrated considerably greater impairment than CHI patients, along with a flat learning/retention curve that showed negligible improvement with repeated trials, recency effects only, and an excessive number of word intrusions (confabulation) on the recognition trial. CHI patients demonstrated both a recency and primacy effect along with improvement over repeated trials (positive slope learning curve). Both groups demonstrated impairment R-O CFD recall; the DAT group again displayed substantially greater copying and recall deficits. Clinical guidelines are given for the use of the R-AVL and R-O CFD for these two patient populations.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Puvenna, V; Engeler, M; Banjara, M; Brennan, C; Schreiber, P; Dadas, A; Bahrami, A; Solanki, J; Bandyopadhyay, A; Morris, J K; Bernick, C; Ghosh, C; Rapp, E; Bazarian, J J; Janigro, D
Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy Journal Article
In: Brain Research, vol. 1630, pp. 225–240, 2016.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult
@article{Puvenna2016,
title = {Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy},
author = {Puvenna, V and Engeler, M and Banjara, M and Brennan, C and Schreiber, P and Dadas, A and Bahrami, A and Solanki, J and Bandyopadhyay, A and Morris, J K and Bernick, C and Ghosh, C and Rapp, E and Bazarian, J J and Janigro, D},
year = {2016},
date = {2016-01-01},
journal = {Brain Research},
volume = {1630},
pages = {225--240},
abstract = {Repetitive traumatic brain injury (rTBI) is one of the major risk factors for the abnormal deposition of phosphorylated tau (PT) in the brain and chronic traumatic encephalopathy (CTE). CTE and temporal lobe epilepsy (TLE) affect the limbic system, but no comparative studies on PT distribution in TLE and CTE are available. It is also unclear whether PT pathology results from repeated head hits (rTBI). These gaps prevent a thorough understanding of the pathogenesis and clinical significance of PT, limiting our ability to develop preventative and therapeutic interventions. We quantified PT in TLE and CTE to unveil whether a history of rTBI is a prerequisite for PT accumulation in the brain. Six postmortem CTE (mean 73.3 years) and age matched control samples were compared to 19 surgically resected TLE brain specimens (4 months-58 years; mean 27.6 years). No history of TBI was present in TLE or control; all CTE patients had a history of rTBI. TLE and CTE brain displayed increased levels of PT as revealed by immunohistochemistry. No age-dependent changes were noted, as PT was present as early as 4 months after birth. In TLE and CTE, cortical neurons, perivascular regions around penetrating pial vessels and meninges were immunopositive for PT; white matter tracts also displayed robust expression of extracellular PT organized in bundles parallel to venules. Microscopically, there were extensive tau-immunoreactive neuronal, astrocytic and degenerating neurites throughout the brain. In CTE perivascular tangles were most prominent. Overall, significant differences in staining intensities were found between CTE and control (P\<0.01) but not between CTE and TLE (P=0.08). pS199 tau analysis showed that CTE had the most high molecular weight tangle-associated tau, whereas epileptic brain contained low molecular weight tau. Tau deposition may not be specific to rTBI since TLE recapitulated most of the pathological features of CTE. Copyright © 2015 Elsevier B.V. All rights reserved.},
keywords = {*Brain Injury, *Brain/me [Metabolism], *Epilepsy/me [Metabolism], *tau Proteins/me [Metabolism], 0 (MAPT protein, 0 (tau Proteins), 80 and over, Adolescent, adult, aged, Brain Injury, Brain/pa [Pathology], Brain/su [Surgery], Child, Chronic/me [Metabolism], Chronic/pa [Pathology], ENZYME-linked immunosorbent assay, Epilepsy/pa [Pathology], Epilepsy/su [Surgery], Female, human), Humans, immunohistochemistry, Infant, Male, middle aged, Phosphorylation, Preschool, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Calcagnile, O; Anell, A; Unden, J
The addition of S100B to guidelines for management of mild head injury is potentially cost saving Journal Article
In: BMC Neurology, vol. 16, no. 1, pp. 200, 2016.
Abstract | BibTeX | Tags: *Brain Concussion/bl [Blood], *Brain Concussion/ec [Economics], *Cost Savings, *Practice Guidelines as Topic, *S100 Calcium Binding Protein beta Subunit/bl [Blo, 0 (Biomarkers), 0 (S100 Calcium Binding Protein beta Subunit), 80 and over, Adolescent, adult, aged, Biomarkers/bl [Blood], Female, Humans, Male, middle aged, SWEDEN, Young Adult
@article{Calcagnile2016,
title = {The addition of S100B to guidelines for management of mild head injury is potentially cost saving},
author = {Calcagnile, O and Anell, A and Unden, J},
year = {2016},
date = {2016-01-01},
journal = {BMC Neurology},
volume = {16},
number = {1},
pages = {200},
abstract = {BACKGROUND: Mild traumatic brain injury (TBI) is associated with substantial costs due to over-triage of patients to computed tomography (CT) scanning, despite validated decision rules. Serum biomarker S100B has shown promise for safely omitting CT scans but the economic impact from clinical use has never been reported. In 2007, S100B was adapted into the existing Scandinavian management guidelines in Halmstad, Sweden, in an attempt to reduce CT scans and save costs. METHODS: Consecutive adult patients with mild TBI (GCS 14-15, loss of consciousness and/or amnesia), managed with the aid of S100B, were prospectively included in this study. Patients were followed up after 3 months with a standardized questionnaire. Theoretical and actual cost differences were calculated. RESULTS: Seven hundred twenty-six patients were included and 29 (4.7 %) showed traumatic abnormalities on CT. No further significant intracranial complications were discovered on follow-up. Two hundred twenty-nine patients (27 %) had normal S100B levels and 497 patients (73 %) showed elevated S100B levels. Over-triage occurred in 73 patients (32 %) and under-triage occurred in 39 patients (7 %). No significant intracranial complications were missed. The introduction of S100B could save 71 per patient if guidelines were strictly followed. As compliance to the guidelines was not perfect, the actual cost saving was 39 per patient. CONCLUSION: Adding S100B to existing guidelines for mild TBI seems to reduce CT usage and costs, especially if guideline compliance could be increased.},
keywords = {*Brain Concussion/bl [Blood], *Brain Concussion/ec [Economics], *Cost Savings, *Practice Guidelines as Topic, *S100 Calcium Binding Protein beta Subunit/bl [Blo, 0 (Biomarkers), 0 (S100 Calcium Binding Protein beta Subunit), 80 and over, Adolescent, adult, aged, Biomarkers/bl [Blood], Female, Humans, Male, middle aged, SWEDEN, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}
Barrio, J R; Small, G W; Wong, K P; Huang, S C; Liu, J; Merrill, D A; Giza, C C; Fitzsimmons, R P; Omalu, B; Bailes, J; Kepe, V
In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344] Journal Article
In: Proceedings of the National Academy of Sciences of the United States of America, vol. 112, no. 16, pp. E2039–47, 2015.
Abstract | BibTeX | Tags: *Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged
@article{Barrio2015,
title = {In vivo characterization of chronic traumatic encephalopathy using [F-18]FDDNP PET brain imaging.[Erratum appears in Proc Natl Acad Sci U S A. 2015 Jun 2;112(22):E2981; PMID: 25964344]},
author = {Barrio, J R and Small, G W and Wong, K P and Huang, S C and Liu, J and Merrill, D A and Giza, C C and Fitzsimmons, R P and Omalu, B and Bailes, J and Kepe, V},
year = {2015},
date = {2015-01-01},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {112},
number = {16},
pages = {E2039--47},
abstract = {Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-beta] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.},
keywords = {*Brain Injury, *Brain/pa [Pathology], *Brain/ri [Radionuclide Imaging], *Nitriles, *Positron-Emission Tomography, 0 (2-(1-(6-((2-fluoroethyl)(methyl)amino)-2-naphth, 0 (Nitriles), 80 and over, adult, aged, Alzheimer Disease/ri [Radionuclide Imaging], Amygdala/mi [Microbiology], Amygdala/pa [Pathology], autopsy, Case-Control Studies, Chronic/ri [Radionuclide Imaging], Demography, Humans, Male, Mesencephalon/mi [Microbiology], Mesencephalon/pa [Pathology], middle aged},
pubstate = {published},
tppubtype = {article}
}
Stein, T D; Montenigro, P H; Alvarez, V E; Xia, W; Crary, J F; Tripodis, Y; Daneshvar, D H; Mez, J; Solomon, T; Meng, G; Kubilus, C A; Cormier, K A; Meng, S; Babcock, K; Kiernan, P; Murphy, L; Nowinski, C J; Martin, B; Dixon, D; Stern, R A; Cantu, R C; Kowall, N W; McKee, A C
Beta-amyloid deposition in chronic traumatic encephalopathy Journal Article
In: Acta Neuropathologica, vol. 130, no. 1, pp. 21–34, 2015.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]
@article{Stein2015b,
title = {Beta-amyloid deposition in chronic traumatic encephalopathy},
author = {Stein, T D and Montenigro, P H and Alvarez, V E and Xia, W and Crary, J F and Tripodis, Y and Daneshvar, D H and Mez, J and Solomon, T and Meng, G and Kubilus, C A and Cormier, K A and Meng, S and Babcock, K and Kiernan, P and Murphy, L and Nowinski, C J and Martin, B and Dixon, D and Stern, R A and Cantu, R C and Kowall, N W and McKee, A C},
year = {2015},
date = {2015-01-01},
journal = {Acta Neuropathologica},
volume = {130},
number = {1},
pages = {21--34},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid beta peptide (Abeta) levels, the extent of Abeta deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Abeta deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Abeta deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Abeta deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p \< 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Abeta plaques and those without. Abeta deposition was significantly associated with the presence of the APOE epsilon4 allele (p = 0.035), older age at symptom onset (p \< 0.001), and older age at death (p \< 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (beta = 2.43},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injury, *Brain/pa [Pathology], *Neurodegenerative Diseases/pa [Pathology], *tau Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (Apolipoprotein E4), 0 (MAPT protein, 0 (tau Proteins), 80 and over, adult, Age Factors, aged, Amyloid/et [Etiology], Amyloid/me [Metabolism], Amyloid/pa [Pathology], Apolipoprotein E4/ge [Genetics], Athletes, Athletic Injuries/ep [Epidemiology], Athletic Injuries/ge [Genetics], Athletic Injuries/me [Metabolism], Athletic Injuries/pa [Pathology], Brain Injury, Brain/me [Metabolism], Chronic/ep [Epidemiology], Chronic/ge [Genetics], Chronic/me [Metabolism], Chronic/pa [Pathology], Cohort Studies, comorbidity, human), Humans, middle aged, Neurodegenerative Diseases/ep [Epidemiology], Neurodegenerative Diseases/ge [Genetics], Neurodegenerative Diseases/me [Metabolism], Plaque, SEVERITY of illness index, veterans, War-Related Injuries/ep [Epidemiology], War-Related Injuries/ge [Genetics], War-Related Injuries/me [Metabolism], War-Related Injuries/pa [Pathology]},
pubstate = {published},
tppubtype = {article}
}
Chetelat, G; Eustache, F; Viader, F; De La Sayette, V; Pelerin, A; Mezenge, F; Hannequin, D; Dupuy, B; Baron, J C; Desgranges, B
FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment Journal Article
In: Neurocase, vol. 11, no. 1, pp. 14–25, 2005.
Abstract | BibTeX | Tags: *Cognition Disorders/dg [Diagnostic Imaging], *Fluorodeoxyglucose F18, *Neuropsychological Tests, *Positron-Emission Tomography, 0Z5B2CJX4D (Fluorodeoxyglucose F18), 80 and over, aged, ANALYSIS of variance, Brain Concussion/dg [Diagnostic Imaging], Brain Concussion/pa [Pathology], BRAIN mapping, Cognition Disorders/di [Diagnosis], Dementia/dg [Diagnostic Imaging], Dementia/di [Diagnosis], Dementia/pp [Physiopathology], Female, Follow-Up Studies, Humans, Male, Memory/ph [Physiology], Mental Status Schedule, middle aged, Predictive Value of Tests, Regression (Psychology), Reproducibility of Results, Time Factors
@article{Chetelat2005,
title = {FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment},
author = {Chetelat, G and Eustache, F and Viader, F and {De La Sayette}, V and Pelerin, A and Mezenge, F and Hannequin, D and Dupuy, B and Baron, J C and Desgranges, B},
year = {2005},
date = {2005-01-01},
journal = {Neurocase},
volume = {11},
number = {1},
pages = {14--25},
abstract = {The accurate prediction, at a pre-dementia stage of Alzheimer's disease (AD), of the subsequent clinical evolution of patients would be a major breakthrough from both therapeutic and research standpoints. Amnestic mild cognitive impairment (MCI) is presently the most common reference to address the pre-dementia stage of AD. However, previous longitudinal studies on patients with MCI assessing neuropsychological and PET markers of future conversion to AD are sparse and yield discrepant findings, while a comprehensive comparison of the relative accuracy of these two categories of measure is still lacking. In the present study, we assessed the global cognitive decline as measured by the Mattis scale in 18 patients with amnestic MCI over an 18-month follow-up period, studying which subtest of this scale showed significant deterioration over time. Using baseline measurements from neuropsychological evaluation of memory and PET, we then assessed significant markers of global cognitive change, that is, percent annual change in the Mattis scale total score, and searched for the best predictor of this global cognitive decline. Altogether, our results revealed significant decline over the 18-month follow-up period in the total score and the verbal initiation and memory-recall subscores of the Mattis scale. The percent annual change in the total Mattis score significantly correlated with age and baseline performances in delayed episodic memory recall as well as semantic autobiographical and category word fluencies. Regarding functional imaging, significant correlations were also found with baseline PET values in the right temporo-parietal and medial frontal areas. Age and right temporo-parietal PET values were the most significant predictors of subsequent global cognitive decline, and the only ones to survive stepwise regression analyses. Our findings are consistent with previous works showing predominant delayed recall and semantic memory impairment at a pre-dementia stage of AD, as well as early metabolic defects in the temporo-parietal associative cortex. However, they suggest that only the latter predictor is specifically and accurately associated with subsequent cognitive decline in patients with MCI within 18 months of first assessment.},
keywords = {*Cognition Disorders/dg [Diagnostic Imaging], *Fluorodeoxyglucose F18, *Neuropsychological Tests, *Positron-Emission Tomography, 0Z5B2CJX4D (Fluorodeoxyglucose F18), 80 and over, aged, ANALYSIS of variance, Brain Concussion/dg [Diagnostic Imaging], Brain Concussion/pa [Pathology], BRAIN mapping, Cognition Disorders/di [Diagnosis], Dementia/dg [Diagnostic Imaging], Dementia/di [Diagnosis], Dementia/pp [Physiopathology], Female, Follow-Up Studies, Humans, Male, Memory/ph [Physiology], Mental Status Schedule, middle aged, Predictive Value of Tests, Regression (Psychology), Reproducibility of Results, Time Factors},
pubstate = {published},
tppubtype = {article}
}
Bigler, E D; Rosa, L; Schultz, F; Hall, S; Harris, J
Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013] Journal Article
In: Journal of Clinical Psychology, vol. 45, no. 2, pp. 277–280, 1989.
Abstract | BibTeX | Tags: *Alzheimer Disease/px [Psychology], *Brain Concussion/px [Psychology], *Form Perception, *MEMORY, *Mental Recall, *Neurocognitive Disorders/px [Psychology], *Neuropsychological Tests, *Pattern Recognition, *Verbal Learning, 80 and over, adult, aged, attention, Female, Humans, Male, middle aged, Psychometrics, SPEECH perception, Visual
@article{Bigler1989,
title = {Rey-Auditory Verbal Learning and Rey-Osterrieth Complex Figure Design performance in Alzheimer's disease and closed head injury.[Erratum appears in J Clin Psychol 1989 Nov;45(6):1013]},
author = {Bigler, E D and Rosa, L and Schultz, F and Hall, S and Harris, J},
year = {1989},
date = {1989-01-01},
journal = {Journal of Clinical Psychology},
volume = {45},
number = {2},
pages = {277--280},
abstract = {Performance on the Rey-Auditory Verbal Learning (R-AVL) and Rey-Osterrieth Complex Figure Design (R-O CFD) tests was examined in patients (N = 94) with dementia of the Alzheimer's type (DAT) and closed head injury (CHI). On the R-AVL, DAT patients demonstrated considerably greater impairment than CHI patients, along with a flat learning/retention curve that showed negligible improvement with repeated trials, recency effects only, and an excessive number of word intrusions (confabulation) on the recognition trial. CHI patients demonstrated both a recency and primacy effect along with improvement over repeated trials (positive slope learning curve). Both groups demonstrated impairment R-O CFD recall; the DAT group again displayed substantially greater copying and recall deficits. Clinical guidelines are given for the use of the R-AVL and R-O CFD for these two patient populations.},
keywords = {*Alzheimer Disease/px [Psychology], *Brain Concussion/px [Psychology], *Form Perception, *MEMORY, *Mental Recall, *Neurocognitive Disorders/px [Psychology], *Neuropsychological Tests, *Pattern Recognition, *Verbal Learning, 80 and over, adult, aged, attention, Female, Humans, Male, middle aged, Psychometrics, SPEECH perception, Visual},
pubstate = {published},
tppubtype = {article}
}