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Article: S100B and S100B autoantibody as biomarkers for early detection of brain metastases in lung cancer.

Choi, Humberto / Puvenna, Vikram / Brennan, Chanda / Mahmoud, Shamseldeen / Wang, Xiao-Feng / Phillips, Michael / Janigro, Damir / Mazzone, Peter

Translational lung cancer research

2016 Volume 5, Issue 4, Page(s) 413–419

Abstract: Background: S100B is an astrocytic protein that enters the blood stream when there is disruption of the blood-brain barrier (BBB). Over time, antibodies against S100B develop in the sera of patients who experience persistent or repeated BBB disruptions. ...

Abstract	Background: S100B is an astrocytic protein that enters the blood stream when there is disruption of the blood-brain barrier (BBB). Over time, antibodies against S100B develop in the sera of patients who experience persistent or repeated BBB disruptions. We explored the use of serum S100B protein and S100B autoantibodies for the detection of brain metastasis in patients with lung cancer. Methods: One hundred and twenty eight untreated patients with lung cancer who had brain imaging performed as part of their routine evaluation, participated. Serum S100B protein levels were measured by direct ELISA and S100B autoantibody levels by reverse ELISA. These levels in patients with brain metastases were compared alone and in combination to those without brain metastases. Results: Eighteen (14%) patients had brain metastasis at the time of lung cancer diagnosis. An S100B cutoff of 0.058 ng/mL had a sensitivity of 89% and specificity of 43% for brain metastasis. When an autoantibody threshold of <2.00 absorbance units was used in conjunction with S100B, the sensitivity remained at 89%, and the specificity increased to 58%. The overall accuracy was 51% with S100B alone, improving to 62.5% when combined with autoantibodies. Conclusions: Serum S100B and S100B autoantibody levels may help to identify which lung cancer patients have brain metastases.
Language	English
Publishing date	2016-08-25
Publishing country	China
Document type	Journal Article
ZDB-ID	2754335-3
ISSN	2226-4477 ; 2218-6751
ISSN (online)	2226-4477
ISSN	2218-6751
DOI	10.21037/tlcr.2016.07.08
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Article ; Online: The role of shear stress in Blood-Brain Barrier endothelial physiology.

Cucullo, Luca / Hossain, Mohammed / Puvenna, Vikram / Marchi, Nicola / Janigro, Damir

BMC neuroscience

2011 Volume 12, Page(s) 40

Abstract: Background: One of the most important and often neglected physiological stimuli contributing to the differentiation of vascular endothelial cells (ECs) into a blood-brain barrier (BBB) phenotype is shear stress (SS). With the use of a well established ... ...

Abstract	Background: One of the most important and often neglected physiological stimuli contributing to the differentiation of vascular endothelial cells (ECs) into a blood-brain barrier (BBB) phenotype is shear stress (SS). With the use of a well established humanized dynamic in vitro BBB model and cDNA microarrays, we have profiled the effect of SS in the induction/suppression of ECs genes and related functions. Results: Specifically, we found a significant upregulation of tight and adherens junctions proteins and genes. Trans-endothelial electrical resistance (TEER) and permeability measurements to know substances have shown that SS promoted the formation of a tight and highly selective BBB. SS also increased the RNA level of multidrug resistance transporters, ion channels, and several p450 enzymes. The RNA level of a number of specialized carrier-mediated transport systems (e.g., glucose, monocarboxylic acid, etc.) was also upregulated.RNA levels of modulatory enzymes of the glycolytic pathway (e.g., lactate dehydrogenase) were downregulated by SS while those involved in the Krebs cycle (e.g., lactate and other dehydrogenases) were upregulated. Measurements of glucose consumption versus lactate production showed that SS negatively modulated the glycolytic bioenergetic pathways of glucose metabolism in favor of the more efficient aerobic respiration. BBB ECs are responsive to inflammatory stimuli. Our data showed that SS increased the RNA levels of integrins and vascular adhesion molecules. SS also inhibited endothelial cell cycle via regulation of BTG family proteins encoding genes. This was paralleled by significant increase in the cytoskeletal protein content while that of membrane, cytosol, and nuclear sub-cellular fractions decreased. Furthermore, analysis of 2D gel electrophoresis (which allows identifying a large number of proteins per sample) of EC proteins extracted from membrane sub-cellular endothelial fractions showed that SS increased the expression levels of tight junction proteins. In addition, regulatory enzymes of the Krebb's cycle (aerobic glucose metabolism) were also upregulated. Furthermore, the expression pattern of key protein regulators of the cell cycle and parallel gene array data supported a cell proliferation inhibitory role for SS. Conclusions: Genomic and proteomic analyses are currently used to examine BBB function in healthy and diseased brain and characterize this dynamic interface. In this study we showed that SS plays a key role in promoting the differentiation of vascular endothelial cells into a truly BBB phenotype. SS affected multiple aspect of the endothelial physiology spanning from tight junctions formation to cell division as well as the expression of multidrug resistance transporters. BBB dysfunction has been observed in many neurological diseases, but the causes are generally unknown. Our study provides essential insights to understand the role played by SS in the BBB formation and maintenance.
MeSH term(s)	Astrocytes/metabolism ; Astrocytes/physiology ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/physiology ; Cell Proliferation ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelial Cells/physiology ; Energy Metabolism ; Gene Expression Regulation ; Glucose/metabolism ; Humans ; Inflammation/metabolism ; Models, Biological ; Stress, Mechanical
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2011-05-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1471-2202
ISSN (online)	1471-2202
DOI	10.1186/1471-2202-12-40
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Article ; Online: Levels of S100B in brain and blood of rats with diabetic ketoacidosis.

Glaser, Nicole / Lo, Weei / Tancredi, Daniel / Orgain, Myra / Puvenna, Vikram / Janigro, Damir / O'Donnell, Martha

Brain research

2015 Volume 1624, Page(s) 536–544

Abstract: Diabetic ketoacidosis (DKA) frequently causes subtle brain injuries in children. Rarely, these injuries can be severe and life threatening. The physiological processes leading to brain injury during DKA are poorly understood. S100B is a calcium-binding ... ...

Abstract	Diabetic ketoacidosis (DKA) frequently causes subtle brain injuries in children. Rarely, these injuries can be severe and life threatening. The physiological processes leading to brain injury during DKA are poorly understood. S100B is a calcium-binding protein secreted by astrocytes. Elevated serum S100B levels are documented in several types of brain injuries. S100B may have either neuroprotective or neurotoxic effects, depending upon the concentration. We undertook the current studies to measure alterations in S100B production and secretion during DKA. We measured serum S100B concentrations in juvenile rats during and after DKA, and used immunohistochemistry to measure S100B expression in the hippocampus, cortex and striatum. Compared to levels in both normal and hyperglycemic control rats, serum S100B levels during DKA were significantly reduced. Serum S100B gradually rose after DKA, returning to levels of hyperglycemic controls by 72 h. S100B expression in the hippocampus was also significantly reduced 24h after DKA. There were no significant changes in S100B expression in other brain regions. Our findings contrast with those for other types of brain injuries in which both serum S100B levels and astrocyte S100B expression are typically elevated. These data suggest that serum S100B measurement cannot be used as an indicator of brain injury during DKA. Whether reduced S100B production or secretion is involved in the pathogenesis of DKA-related brain injury should be investigated.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/toxicity ; Brain/metabolism ; Brain/pathology ; Diabetic Ketoacidosis/blood ; Diabetic Ketoacidosis/chemically induced ; Diabetic Ketoacidosis/pathology ; Disease Models, Animal ; Glial Fibrillary Acidic Protein/metabolism ; Hyperglycemia/blood ; Hyperglycemia/etiology ; Hyperglycemia/pathology ; Rats ; Rats, Sprague-Dawley ; S100 Calcium Binding Protein beta Subunit/metabolism ; Streptozocin/toxicity ; Time Factors
Chemical Substances	Antibiotics, Antineoplastic ; Glial Fibrillary Acidic Protein ; S100 Calcium Binding Protein beta Subunit ; Streptozocin (5W494URQ81)
Language	English
Publishing date	2015-10-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2015.07.044
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Article ; Online: The etiological role of blood-brain barrier dysfunction in seizure disorders.

Marchi, Nicola / Tierney, William / Alexopoulos, Andreas V / Puvenna, Vikram / Granata, Tiziana / Janigro, Damir

Cardiovascular psychiatry and neurology

2011 Volume 2011, Page(s) 482415

Abstract: A wind of change characterizes epilepsy research efforts. The traditional approach, based on a neurocentric view of seizure generation, promoted understanding of the neuronal mechanisms of seizures; this resulted in the development of potent anti- ... ...

Abstract	A wind of change characterizes epilepsy research efforts. The traditional approach, based on a neurocentric view of seizure generation, promoted understanding of the neuronal mechanisms of seizures; this resulted in the development of potent anti-epileptic drugs (AEDs). The fact that a significant number of individuals with epilepsy still fail to respond to available AEDs restates the need for an alternative approach. Blood-brain barrier (BBB) dysfunction is an important etiological player in seizure disorders, and combination therapies utilizing an AED in conjunction with a "cerebrovascular" drug could be used to control seizures more effectively than AED therapy alone. The fact that the BBB plays an etiologic role in other neurological diseases will be discussed in the context of a more "holistic" approach to the patient with epilepsy, where comorbidity variables are also encompassed by drug therapy.
Language	English
Publishing date	2011-03-30
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2514153-3
ISSN	2090-0171 ; 2090-0163
ISSN (online)	2090-0171
ISSN	2090-0163
DOI	10.1155/2011/482415
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Article ; Online: The role of shear stress in Blood-Brain Barrier endothelial physiology

Puvenna Vikram / Hossain Mohammed / Cucullo Luca / Marchi Nicola / Janigro Damir

BMC Neuroscience, Vol 12, Iss 1, p

2011 Volume 40

Abstract: Abstract Background One of the most important and often neglected physiological stimuli contributing to the differentiation of vascular endothelial cells (ECs) into a blood-brain barrier (BBB) phenotype is shear stress (SS). With the use of a well ... ...

Abstract	Abstract Background One of the most important and often neglected physiological stimuli contributing to the differentiation of vascular endothelial cells (ECs) into a blood-brain barrier (BBB) phenotype is shear stress (SS). With the use of a well established humanized dynamic in vitro BBB model and cDNA microarrays, we have profiled the effect of SS in the induction/suppression of ECs genes and related functions. Results Specifically, we found a significant upregulation of tight and adherens junctions proteins and genes. Trans-endothelial electrical resistance (TEER) and permeability measurements to know substances have shown that SS promoted the formation of a tight and highly selective BBB. SS also increased the RNA level of multidrug resistance transporters, ion channels, and several p450 enzymes. The RNA level of a number of specialized carrier-mediated transport systems (e.g., glucose, monocarboxylic acid, etc.) was also upregulated. RNA levels of modulatory enzymes of the glycolytic pathway (e.g., lactate dehydrogenase) were downregulated by SS while those involved in the Krebs cycle (e.g., lactate and other dehydrogenases) were upregulated. Measurements of glucose consumption versus lactate production showed that SS negatively modulated the glycolytic bioenergetic pathways of glucose metabolism in favor of the more efficient aerobic respiration. BBB ECs are responsive to inflammatory stimuli. Our data showed that SS increased the RNA levels of integrins and vascular adhesion molecules. SS also inhibited endothelial cell cycle via regulation of BTG family proteins encoding genes. This was paralleled by significant increase in the cytoskeletal protein content while that of membrane, cytosol, and nuclear sub-cellular fractions decreased. Furthermore, analysis of 2D gel electrophoresis (which allows identifying a large number of proteins per sample) of EC proteins extracted from membrane sub-cellular endothelial fractions showed that SS increased the expression levels of tight junction proteins. In addition, regulatory enzymes of the Krebb's cycle (aerobic glucose metabolism) were also upregulated. Furthermore, the expression pattern of key protein regulators of the cell cycle and parallel gene array data supported a cell proliferation inhibitory role for SS. Conclusions Genomic and proteomic analyses are currently used to examine BBB function in healthy and diseased brain and characterize this dynamic interface. In this study we showed that SS plays a key role in promoting the differentiation of vascular endothelial cells into a truly BBB phenotype. SS affected multiple aspect of the endothelial physiology spanning from tight junctions formation to cell division as well as the expression of multidrug resistance transporters. BBB dysfunction has been observed in many neurological diseases, but the causes are generally unknown. Our study provides essential insights to understand the role played by SS in the BBB formation and maintenance.
Keywords	Cerebral blood flow ; Shear stress ; Cell Cycle ; Alternative ; In vitro ; Inflammation ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Neurophysiology and neuropsychology ; QP351-495
Subject code	570
Language	English
Publishing date	2011-05-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Significance of ubiquitin carboxy-terminal hydrolase L1 elevations in athletes after sub-concussive head hits.

Puvenna, Vikram / Brennan, Chanda / Shaw, Gerald / Yang, Cui / Marchi, Nicola / Bazarian, Jeffrey J / Merchant-Borna, Kian / Janigro, Damir

PloS one

2014 Volume 9, Issue 5, Page(s) e96296

Abstract: The impact of sub-concussive head hits (sub-CHIs) has been recently investigated in American football players, a population at risk for varying degrees of post-traumatic sequelae. Results show how sub-CHIs in athletes translate in serum as the appearance ...

Abstract	The impact of sub-concussive head hits (sub-CHIs) has been recently investigated in American football players, a population at risk for varying degrees of post-traumatic sequelae. Results show how sub-CHIs in athletes translate in serum as the appearance of reporters of blood-brain barrier disruption (BBBD), how the number and severity of sub-CHIs correlate with elevations of putative markers of brain injury is unknown. Serum brain injury markers such as UCH-L1 depend on BBBD. We investigated the effects of sub-CHIs in collegiate football players on markers of BBBD, markers of cerebrospinal fluid leakage (serum beta 2-transferrin) and markers of brain damage. Emergency room patients admitted for a clinically-diagnosed mild traumatic brain injury (mTBI) were used as positive controls. Healthy volunteers were used as negative controls. Specifically this study was designed to determine the use of UCH-L1 as an aid in the diagnosis of sub-concussive head injury in athletes. The extent and intensity of head impacts and serum values of S100B, UCH-L1, and beta-2 transferrin were measured pre- and post-game from 15 college football players who did not experience a concussion after a game. S100B was elevated in players experiencing the most sub-CHIs; UCH-L1 levels were also elevated but did not correlate with S100B or sub-CHIs. Beta-2 transferrin levels remained unchanged. No correlation between UCH-L1 levels and mTBI were measured in patients. Low levels of S100B were able to rule out mTBI and high S100B levels correlated with TBI severity. UCH-L1 did not display any interpretable change in football players or in individuals with mild TBI. The significance of UCH-L1 changes in sub-concussions or mTBI needs to be further elucidated.
MeSH term(s)	Athletes/statistics & numerical data ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/pathology ; Brain Concussion/blood ; Brain Concussion/enzymology ; Brain Concussion/metabolism ; Brain Injuries/blood ; Brain Injuries/enzymology ; Brain Injuries/metabolism ; Enzyme-Linked Immunosorbent Assay ; Humans ; S100 Calcium Binding Protein beta Subunit/blood ; Transferrin/metabolism ; Ubiquitin Thiolesterase/blood ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	S100 Calcium Binding Protein beta Subunit ; S100B protein, human ; Transferrin ; UCHL1 protein, human ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2014-05-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0096296
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Article ; Online: Blood-brain barrier P450 enzymes and multidrug transporters in drug resistance: a synergistic role in neurological diseases.

Ghosh, Chaitali / Puvenna, Vikram / Gonzalez-Martinez, Jorge / Janigro, Damir / Marchi, Nicola

Current drug metabolism

2011 Volume 12, Issue 8, Page(s) 742–749

Abstract: Drug penetration into the central nervous system (CNS) is controlled by the blood-brain barrier (BBB). Even though a number of strategies to circumvent the BBB and to improve drug access have been developed, drug resistance in CNS diseases remains an ... ...

Abstract	Drug penetration into the central nervous system (CNS) is controlled by the blood-brain barrier (BBB). Even though a number of strategies to circumvent the BBB and to improve drug access have been developed, drug resistance in CNS diseases remains an unmet clinical problem. We here review the mechanisms by which a healthy or pathological BBB influences drug distribution in the brain, with emphasis on the role of P450 metabolic enzymes and multi-drug transporter (MDT) proteins. In addition to the classic hepatic and gut biotransformation pathways, CNS expression of P450 enzymes may bear pharmacokinetic and pharmacodynamic significance exerting a metabolic activity and transforming parent drugs into specific products. We propose these mechanisms to play a major role in CNS drug resistant pathologies including refractory forms of epilepsy. Changes in the cerebrovascular hemodynamic conditions can affect expression of P450 enzymes and MDT proteins. This should be taken into account when developing in vitro experimental approaches to reproduce the physiological or pathological properties of the BBB. Finally, a link between P450 and MDT expression in the diseased brain and cell survival is discussed.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Brain/metabolism ; Brain/physiopathology ; Cell Survival ; Central Nervous System Agents/pharmacokinetics ; Central Nervous System Agents/pharmacology ; Cytochrome P-450 Enzyme System/genetics ; Cytochrome P-450 Enzyme System/metabolism ; Drug Resistance ; Gene Expression Regulation ; Hemodynamics ; Humans ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/metabolism ; Nervous System Diseases/drug therapy ; Nervous System Diseases/physiopathology
Chemical Substances	Central Nervous System Agents ; Membrane Transport Proteins ; Cytochrome P-450 Enzyme System (9035-51-2)
Language	English
Publishing date	2011-06-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2064815-7
ISSN	1875-5453 ; 1389-2002
ISSN (online)	1875-5453
ISSN	1389-2002
DOI	10.2174/138920011798357051
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Article ; Online: Pathophysiological impact of cigarette smoke exposure on the cerebrovascular system with a focus on the blood-brain barrier: expanding the awareness of smoking toxicity in an underappreciated area.

Mazzone, Peter / Tierney, William / Hossain, Mohammed / Puvenna, Vikram / Janigro, Damir / Cucullo, Luca

International journal of environmental research and public health

2010 Volume 7, Issue 12, Page(s) 4111–4126

Abstract: Recent evidence has indicated that active and passive cigarette smoking are associated, in a dose-dependent manner, with dysfunction of normal endothelial physiology. Tobacco smoke (TS) may predispose individuals to atherogenic and thrombotic problems, ... ...

Abstract	Recent evidence has indicated that active and passive cigarette smoking are associated, in a dose-dependent manner, with dysfunction of normal endothelial physiology. Tobacco smoke (TS) may predispose individuals to atherogenic and thrombotic problems, significantly increasing the risk for ischemic manifestations such as acute coronary syndrome and stroke. Despite the strong evidence for an association between smoking and vascular impairment, the impact of TS exposure on the blood-brain barrier (BBB) has only been marginally addressed. This is a major problem given that the BBB is crucial in the maintenance of brain homeostasis. Recent data have also shown that chronic smokers have a higher incidence of small vessel ischemic disease (SVID), a pathological condition characterized by leaky brain microvessels and loss of BBB integrity. In the brain TS increases the risk of silent cerebral infarction (SCI) and stroke owing to the pro-coagulant and atherogenic effects of smoking. In this article we provide a detailed review and analysis of current knowledge of the pathophysiology of tobacco smoke toxicity at the cerebrovascular levels. We also discuss the potential toxicity of recently marketed "potential-reduced exposure products".
MeSH term(s)	Blood-Brain Barrier/physiopathology ; Cerebrovascular Disorders/epidemiology ; Cerebrovascular Disorders/etiology ; Cerebrovascular Disorders/immunology ; Cerebrovascular Disorders/physiopathology ; Endothelium, Vascular/physiopathology ; Humans ; Smoking/physiopathology ; Tobacco Smoke Pollution/adverse effects
Chemical Substances	Tobacco Smoke Pollution
Language	English
Publishing date	2010-11-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2175195-X
ISSN	1660-4601 ; 1661-7827
ISSN (online)	1660-4601
ISSN	1661-7827
DOI	10.3390/ijerph7124111
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Article ; Online: The Etiological Role of Blood-Brain Barrier Dysfunction in Seizure Disorders

Nicola Marchi / William Tierney / Andreas V. Alexopoulos / Vikram Puvenna / Tiziana Granata / Damir Janigro

Cardiovascular Psychiatry and Neurology, Vol

2011 Volume 2011

Keywords	Neurology. Diseases of the nervous system ; RC346-429 ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Neurology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; DOAJ:Cardiovascular
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Is phosphorylated tau unique to chronic traumatic encephalopathy? Phosphorylated tau in epileptic brain and chronic traumatic encephalopathy.

Puvenna, Vikram / Engeler, Madeline / Banjara, Manoj / Brennan, Chanda / Schreiber, Peter / Dadas, Aaron / Bahrami, Ashkon / Solanki, Jesal / Bandyopadhyay, Anasua / Morris, Jacqueline K / Bernick, Charles / Ghosh, Chaitali / Rapp, Edward / Bazarian, Jeffrey J / Janigro, Damir

Brain research

2016 Volume 1630, Page(s) 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 ... ...

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.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Brain/metabolism ; Brain/pathology ; Brain/surgery ; Brain Injury, Chronic/metabolism ; Brain Injury, Chronic/pathology ; Child ; Child, Preschool ; Enzyme-Linked Immunosorbent Assay ; Epilepsy/metabolism ; Epilepsy/pathology ; Epilepsy/surgery ; Female ; Humans ; Immunohistochemistry ; Infant ; Male ; Middle Aged ; Phosphorylation ; Young Adult ; tau Proteins/metabolism
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2016-01-01
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2015.11.007
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