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Article ; Online: The role and diagnostic significance of cellular barriers after concussive head trauma.

Dadas, Aaron / Janigro, Damir

Concussion (London, England)

2018 Volume 3, Issue 1, Page(s) CNC53

Abstract: The onset of concussive head trauma often triggers an intricate sequence of physical consequences and pathophysiological responses. These sequelae can be acute (i.e., hematoma) or chronic (i.e., autoimmune response, neurodegeneration, etc.), and may ... ...

Abstract	The onset of concussive head trauma often triggers an intricate sequence of physical consequences and pathophysiological responses. These sequelae can be acute (i.e., hematoma) or chronic (i.e., autoimmune response, neurodegeneration, etc.), and may follow traumas of any severity. A critical factor for prognostication of postconcussion outcome is the pathophysiological response of cellular barriers, which can be measured by several biomarkers of the acute and chronic postinjury phases. We present herein a review on the postconcussion mechanisms of the blood-brain barrier, as well as the diagnostic/prognostic approaches that utilize differential biomarker expression across this boundary. We discuss the role of the blood-saliva cellular barrier as a regulatory filter for brain-derived biomarkers in blood, and its implications for saliva-based diagnostic assays.
Language	English
Publishing date	2018-01-31
Publishing country	England
Document type	Journal Article ; Review
ISSN	2056-3299
ISSN (online)	2056-3299
DOI	10.2217/cnc-2017-0019
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Article ; Online: Breakdown of blood brain barrier as a mechanism of post-traumatic epilepsy.

Dadas, Aaron / Janigro, Damir

Neurobiology of disease

2018 Volume 123, Page(s) 20–26

Abstract: Traumatic brain injury (TBI) accounts for approximately 16% of acute symptomatic seizures which usually occur in the first week after trauma. Children are at higher risk for post-traumatic seizures than adults. Post-traumatic seizures are a risk factor ... ...

Abstract	Traumatic brain injury (TBI) accounts for approximately 16% of acute symptomatic seizures which usually occur in the first week after trauma. Children are at higher risk for post-traumatic seizures than adults. Post-traumatic seizures are a risk factor for delayed development of epilepsy. Delayed, chronic post-traumatic epilepsy is preceded by a silent period during which therapeutic interventions may arrest, revert or prevent epileptogenesis. A number of recent review articles summarize the most important features of post-traumatic seizures and epilepsy; this review will instead focus on the link between cerebrovascular permeability, epileptogenesis and ictal events after TBI. The possibility of acting on the blood-brain barrier (BBB) and the neurovascular unit to prevent, disrupt or treat post-traumatic epilepsy is also discussed. Finally, we describe the latest quest for biomarkers of epileptogenesis which may allow for a more targeted intervention.
MeSH term(s)	Animals ; Biomarkers ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/physiopathology ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/diagnosis ; Brain Injuries, Traumatic/metabolism ; Capillary Permeability ; Epilepsy, Post-Traumatic/diagnosis ; Epilepsy, Post-Traumatic/etiology ; Epilepsy, Post-Traumatic/metabolism ; Humans
Chemical Substances	Biomarkers
Language	English
Publishing date	2018-07-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2018.06.022
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Article: Biomarkers in traumatic brain injury (TBI): a review.

Dadas, Aaron / Washington, Jolewis / Diaz-Arrastia, Ramon / Janigro, Damir

Neuropsychiatric disease and treatment

2018 Volume 14, Page(s) 2989–3000

Abstract: Biomarkers can be broadly defined as qualitative or quantitative measurements that convey information on the physiopathological state of a subject at a certain time point or disease state. Biomarkers can indicate health, pathology, or response to ... ...

Abstract	Biomarkers can be broadly defined as qualitative or quantitative measurements that convey information on the physiopathological state of a subject at a certain time point or disease state. Biomarkers can indicate health, pathology, or response to treatment, including unwanted side effects. When used as outcomes in clinical trials, biomarkers act as surrogates or substitutes for clinically meaningful endpoints. Biomarkers of disease can be diagnostic (the identification of the nature and cause of a condition) or prognostic (predicting the likelihood of a person's survival or outcome of a disease). In addition, genetic biomarkers can be used to quantify the risk of developing a certain disease. In the specific case of traumatic brain injury, surrogate blood biomarkers of imaging can improve the standard of care and reduce the costs of diagnosis. In addition, a prognostic role for biomarkers has been suggested in the case of post-traumatic epilepsy. Given the extensive literature on clinical biomarkers, we will focus herein on biomarkers which are present in peripheral body fluids such as saliva and blood. In particular, blood biomarkers, such as glial fibrillary acidic protein and salivary/blood S100B, will be discussed together with the use of nucleic acids (eg, DNA) collected from peripheral cells.
Language	English
Publishing date	2018-11-08
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2186503-6
ISSN	1178-2021 ; 1176-6328
ISSN (online)	1178-2021
ISSN	1176-6328
DOI	10.2147/NDT.S125620
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Article: Cerebral Waste Accumulation and Glymphatic Clearance as Mechanisms of Human Neurological Diseases.

Dadas, Aaron / Washington, Jolewis / Janigro, Damir

Journal of neurology & neuromedicine

2016 Volume 1, Issue 7, Page(s) 15–19

Abstract: The brain is a complex system that requires continual regulation of parenchymal pressure, osmolarity, and waste removal for optimal function; despite this, human brain lacks any obvious extension of lymphatic circulation for moderating fluid and waste ... ...

Abstract	The brain is a complex system that requires continual regulation of parenchymal pressure, osmolarity, and waste removal for optimal function; despite this, human brain lacks any obvious extension of lymphatic circulation for moderating fluid and waste regulation. We recapitulate herein a recent analysis of proteinaceous waste deposition in the human brain, its observed route of clearance, and the implications of abnormal accumulation along this clearance pathway as a potential mechanism of neurological diseases. This study uncovered an analogous staining pattern of cerebral phosphorylated tau in temporal lobe epilepsy (TLE) and chronic traumatic encephalopathy (CTE). Regardless of the underlying physiopathology, p-tau elimination occurred via circulation through the perivenous space, as predicted by a glymphatic route of clearance. Remarkably, we demonstrated that p-tau is associated with a neurological disease that can develop independent of head trauma, since in both CTE and TLE: 1) Extracellular p-tau followed unidirectional, fluid-driven pathways that led toward the space bordering large (>100 μm diameter) blood vessels; 2) Tau-positive staining occurred within astroglial cells adjacent to blood vessels, which signified transcellular transport of p-tau as a potential secondary efflux route; 3) P-tau frequently appeared clustered within the perivenous space. This waste aggregation bears significant implications in the disruption of interstitial fluid circulation, which may contribute to exacerbation of disease states. A better understanding of waste elimination in the human brain may prove significant as a therapeutic target to improve parenchymal fluid circulation, and consequently, mitigate the hydrostatic, osmotic and oncotic imbalances that often cause or exacerbate brain diseases.
Language	English
Publishing date	2016-10-15
Publishing country	United States
Document type	Journal Article
ISSN	2572-942X
ISSN	2572-942X
DOI	10.29245/2572.942X/2016/7.1082
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Article ; Online: Improving the clinical management of traumatic brain injury through the pharmacokinetic modeling of peripheral blood biomarkers.

Dadas, Aaron / Washington, Jolewis / Marchi, Nicola / Janigro, Damir

Fluids and barriers of the CNS

2016 Volume 13, Issue 1, Page(s) 21

Abstract: Background: Blood biomarkers of neurovascular damage are used clinically to diagnose the presence severity or absence of neurological diseases, but data interpretation is confounded by a limited understanding of their dependence on variables other than ... ...

Abstract	Background: Blood biomarkers of neurovascular damage are used clinically to diagnose the presence severity or absence of neurological diseases, but data interpretation is confounded by a limited understanding of their dependence on variables other than the disease condition itself. These include half-life in blood, molecular weight, and marker-specific biophysical properties, as well as the effects of glomerular filtration, age, gender, and ethnicity. To study these factors, and to provide a method for markers' analyses, we developed a kinetic model that allows the integrated interpretation of these properties. Methods: The pharmacokinetic behaviors of S100B (monomer and homodimer), Glial Fibrillary Acidic Protein and Ubiquitin C-Terminal Hydrolase L1 were modeled using relevant chemical and physical properties; modeling results were validated by comparison with data obtained from healthy subjects or individuals affected by neurological diseases. Brain imaging data were used to model passage of biomarkers across the blood-brain barrier. Results: Our results show the following: (1) changes in biomarker serum levels due to age or disease progression are accounted for by differences in kidney filtration; (2) a significant change in the brain-to-blood volumetric ratio, which is characteristic of infant and adult development, contributes to variation in blood concentration of biomarkers; (3) the effects of extracranial contribution at steady-state are predicted in our model to be less important than suspected, while the contribution of blood-brain barrier disruption is confirmed as a significant factor in controlling markers' appearance in blood, where the biomarkers are typically detected; (4) the contribution of skin to the marker S100B blood levels depends on a direct correlation with pigmentation and not ethnicity; the contribution of extracranial sources for other markers requires further investigation. Conclusions: We developed a multi-compartment, pharmacokinetic model that integrates the biophysical properties of a given brain molecule and predicts its time-dependent concentration in blood, for populations of varying physical and anatomical characteristics. This model emphasizes the importance of the blood-brain barrier as a gatekeeper for markers' blood appearance and, ultimately, for rational clinical use of peripherally-detected brain protein.
MeSH term(s)	Aging/blood ; Biomarkers/blood ; Blood-Brain Barrier/diagnostic imaging ; Blood-Brain Barrier/metabolism ; Brain Injuries, Traumatic/blood ; Brain Injuries, Traumatic/therapy ; Continental Population Groups ; Disease Management ; Disease Progression ; Female ; Glial Fibrillary Acidic Protein/blood ; Humans ; Infant, Newborn ; Kidney/metabolism ; Male ; Middle Aged ; Models, Cardiovascular ; Prospective Studies ; S100 Calcium Binding Protein beta Subunit/blood ; Seasons ; Skin/metabolism ; Skin Pigmentation/physiology ; Ubiquitin Thiolesterase/blood
Chemical Substances	Biomarkers ; Glial Fibrillary Acidic Protein ; S100 Calcium Binding Protein beta Subunit ; S100B protein, human ; UCHL1 protein, human ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2016-11-30
Publishing country	England
Document type	Journal Article ; Validation Studies
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-016-0045-y
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Article ; Online: Detection of brain-directed autoantibodies in the serum of non-small cell lung cancer patients.

Banjara, Manoj / Ghosh, Chaitali / Dadas, Aaron / Mazzone, Peter / Janigro, Damir

PloS one

2017 Volume 12, Issue 7, Page(s) e0181409

Abstract: Antibodies against brain proteins were identified in the plasma of cancer patients and are defined to cause paraneoplastic neurological syndromes. The profiles of brain-directed antibodies in non-small cell lung cancer (NSCLC) are largely unknown. Here, ... ...

Abstract	Antibodies against brain proteins were identified in the plasma of cancer patients and are defined to cause paraneoplastic neurological syndromes. The profiles of brain-directed antibodies in non-small cell lung cancer (NSCLC) are largely unknown. Here, for the first time, we compared autoantibodies against brain proteins in NSCLC (n = 18) against those present in age-matched non-cancer control subjects (n = 18) with a similar life-style, habit, and medical history. Self-recognizing immunoglobulin (IgG) are primarily directed against cells in the cortex (P = 0.008), hippocampus (P = 0.003-0.05), and cerebellum (P = 0.02). More specifically, IgG targets were prominent in the pyramidal, Purkinje, and granule cell layers. Furthermore, autoimmune IgG signals were localized to neurons (81%), astrocytes (48%), and endothelial (29%) cells. While cancer sera yielded overall higher intensity signals, autoantigens of 100, 65, 45, 37, and 30 kDa molecular weights were the most represented. Additionally, a group of 100 kDa proteins seem more prevalent in female adenocarcinoma patients (4/5, 80%). In conclusion, our results revealed autoantigen specificity in NSCLC, which implicitly depends on patient's demographics and disease history. Patients at risk for lung cancer but with no active disease revealed that the immune profile in NSCLC is disease-dependent.
MeSH term(s)	Adenocarcinoma/blood ; Adenocarcinoma/immunology ; Aged ; Aged, 80 and over ; Animals ; Antigens, Nuclear/immunology ; Astrocytes/immunology ; Autoantibodies/blood ; Autoantibodies/immunology ; Autoantigens/chemistry ; Autoantigens/immunology ; Blotting, Western ; Brain/immunology ; Carcinoma, Non-Small-Cell Lung/blood ; Carcinoma, Non-Small-Cell Lung/immunology ; Female ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Immunohistochemistry ; Lung Neoplasms/blood ; Lung Neoplasms/immunology ; Male ; Middle Aged ; Molecular Weight ; Nerve Tissue Proteins/immunology ; Neurons/immunology ; Purkinje Cells/immunology ; Pyramidal Cells/immunology ; Rats, Sprague-Dawley
Chemical Substances	Antigens, Nuclear ; Autoantibodies ; Autoantigens ; Immunoglobulin G ; Nerve Tissue Proteins ; neuronal nuclear antigen NeuN, human
Language	English
Publishing date	2017-07-26
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0181409
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Article ; Online: Pathophysiological implications of neurovascular P450 in brain disorders.

Ghosh, Chaitali / Hossain, Mohammed / Solanki, Jesal / Dadas, Aaron / Marchi, Nicola / Janigro, Damir

Drug discovery today

2016 Volume 21, Issue 10, Page(s) 1609–1619

Abstract: Over the past decades, the significance of cytochrome P450 (CYP) enzymes has expanded beyond their role as peripheral drug metabolizers in the liver and gut. CYP enzymes are also functionally active at the neurovascular interface. CYP expression is ... ...

Abstract	Over the past decades, the significance of cytochrome P450 (CYP) enzymes has expanded beyond their role as peripheral drug metabolizers in the liver and gut. CYP enzymes are also functionally active at the neurovascular interface. CYP expression is modulated by disease states, impacting cellular functions, detoxification, and reactivity to toxic stimuli and brain drug biotransformation. Unveiling the physiological and molecular complexity of brain P450 enzymes will improve our understanding of the mechanisms underlying brain drug availability, pharmacological efficacy, and neurotoxic adverse effects from pharmacotherapy targeting brain disorders.
MeSH term(s)	Animals ; Biotransformation ; Brain/metabolism ; Brain Diseases/metabolism ; Cytochrome P-450 Enzyme System/metabolism ; Drug Discovery ; Drug Interactions ; Humans
Chemical Substances	Cytochrome P-450 Enzyme System (9035-51-2)
Language	English
Publishing date	2016-06-14
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2016.06.004
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Zs.A 4725: Show issues

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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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