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Article: Immune, RNA, and Neurocognitive Genetic Networks in Bipolar Disorder Subtypes: A Transcriptomic Meta-Analysis.

Jang, Tyler / Kaul, Marcus

Research square

2024

Abstract: Background: Little is known about the pathogenesis of Bipolar Disorder, and even less is known about the genetic differences between its subtypes. Bipolar Disorder is classified into different subtypes, which present different symptoms and lifetime ... ...

Abstract	Background: Little is known about the pathogenesis of Bipolar Disorder, and even less is known about the genetic differences between its subtypes. Bipolar Disorder is classified into different subtypes, which present different symptoms and lifetime courses. While genetic studies have been conducted in Bipolar Disorder, most examined the gene expression of only Bipolar Disorder Type 1. Studies that include Bipolar Disorder Type 1 and Bipolar Disorder Type 2 often fail to differentiate them into separate conditions. Few large transcriptomic meta-analyses in Bipolar Disorder have been conducted to identify genetic pathways. Thus, using publicly available data sets we aim here to uncover significant differential gene expression that allows distinguishing Type 1 and Type 2 Bipolar Disorders, as well as find patterns in Bipolar Disorder as a whole. Methods: We analyze 17 different gene expression data sets from different tissue in Bipolar Disorder using GEO2R and manual analysis, of which 15 contained significant differential gene expression results. We use STRING and Cytoscape to examine Gene Ontology to find significantly affected genetic pathways. We identify hub genes using cytoHubba, a plugin in Cytoscape. We find genes common to data sets of the same material or subtype. Results: 12 out of 15 data sets are enriched for immune system and RNA related pathways. 9 out of 15 data sets are enriched for neurocognitive and metal ion related GO terms. Analysis of Bipolar Disorder Type 1 vs Bipolar Disorder Type 2 revealed most differentially expressed genes were related to immune function, especially cytokines. Terms related to synaptic signaling and neurotransmitter secretion were found in down-regulated GO terms while terms related to neuron apoptosis and death were up-regulated. We identify the gene SNCA as a potential biomarker for overall Bipolar Disorder diagnosis due to its prevalence in our data sets. Conclusions: The immune system and RNA related pathways are significantly enriched across the Bipolar Disorder data sets. The role of these pathways is likely more critically important to the function of Bipolar Disorder than currently understood. Further studies should clearly label the subtype of Bipolar Disorder used in their research and more effort needs to be undertaken to collect samples from Cyclothymic Disorder and Bipolar Disorder Type 2.
Language	English
Publishing date	2024-01-17
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3508951/v1
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Article ; Online: The 23rd Scientific Conference of the Society on Neuroimmune Pharmacology.

Kaul, Marcus

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2017 Volume 12, Issue Suppl 1, Page(s) 1–2

Abstract: The 23rd Scientific Conference of the Society on Neuroimmune Pharmacology (SNIP) will take place in Philadelphia, PA, USA, from March 29 to April 1, 2017. The conference will present a selection of the latest and most advanced research in the ... ...

Abstract	The 23rd Scientific Conference of the Society on Neuroimmune Pharmacology (SNIP) will take place in Philadelphia, PA, USA, from March 29 to April 1, 2017. The conference will present a selection of the latest and most advanced research in the intersecting areas of neuroscience, immunology, pharmacology and its translational aspects.
MeSH term(s)	Animals ; Congresses as Topic/trends ; Humans ; Neuroimmunomodulation/drug effects ; Neuroimmunomodulation/immunology ; Neurosciences/methods ; Neurosciences/trends ; Pharmacology/methods ; Pharmacology/trends ; Philadelphia ; Societies, Scientific/trends
Language	English
Publishing date	2017-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-017-9737-6
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Article: Transcriptomic and Genetic Profiling of HIV-Associated Neurocognitive Disorders.

Ojeda-Juárez, Daniel / Kaul, Marcus

Frontiers in molecular biosciences

2021 Volume 8, Page(s) 721954

Abstract: Early in the HIV pandemic, it became evident that people living with HIV (PLWH) develop a wide range of neurological and neurocognitive complications. Even after the introduction of combination antiretroviral therapy (cART), which dramatically improved ... ...

Abstract	Early in the HIV pandemic, it became evident that people living with HIV (PLWH) develop a wide range of neurological and neurocognitive complications. Even after the introduction of combination antiretroviral therapy (cART), which dramatically improved survival of PLWH, the overall number of people living with some form of HIV-associated neurocognitive disorders (HAND) seemed to remain unchanged, although the incidence of dementia declined and questions about the incidence and diagnosis of the mildest form of HAND arose. To better understand this complex disease, several transcriptomic analyses have been conducted in autopsy samples, as well as in non-human primates and small animal rodent models. However, genetic studies in the HIV field have mostly focused on the genetic makeup of the immune system. Much less is known about the genetic underpinnings of HAND. Here, we provide a summary of reported transcriptomic and epigenetic changes in HAND, as well as some of the potential genetic underpinnings that have been linked to HAND, and discuss future directions with hurdles to overcome and angles that remain to be explored.
Language	English
Publishing date	2021-10-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2021.721954
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Article ; Online: Interferon-β deficiency alters brain response to chronic HIV-1 envelope protein exposure in a transgenic model of NeuroHIV.

Singh, Hina / Koury, Jeffrey / Maung, Ricky / Roberts, Amanda J / Kaul, Marcus

Brain, behavior, and immunity

2024 Volume 118, Page(s) 1–21

Abstract: Human immunodeficiency virus-1 (HIV-1) infects the central nervous system (CNS) and causes HIV-associated neurocognitive disorders (HAND) in about half of the population living with the virus despite combination anti-retroviral therapy (cART). HIV-1 ... ...

Abstract	Human immunodeficiency virus-1 (HIV-1) infects the central nervous system (CNS) and causes HIV-associated neurocognitive disorders (HAND) in about half of the population living with the virus despite combination anti-retroviral therapy (cART). HIV-1 activates the innate immune system, including the production of type 1 interferons (IFNs) α and β. Transgenic mice expressing HIV-1 envelope glycoprotein gp120 (HIVgp120tg) in the CNS develop memory impairment and share key neuropathological features and differential CNS gene expression with HIV patients, including the induction of IFN-stimulated genes (ISG). Here we show that knocking out IFNβ (IFNβKO) in HIVgp120tg and non-tg control mice impairs recognition and spatial memory, but does not affect anxiety-like behavior, locomotion, or vision. The neuropathology of HIVgp120tg mice is only moderately affected by the KO of IFNβ but in a sex-dependent fashion. Notably, in cerebral cortex of IFNβKO animals presynaptic terminals are reduced in males while neuronal dendrites are reduced in females. The IFNβKO results in the hippocampal CA1 region of both male and female HIVgp120tg mice in an ameliorated loss of neuronal presynaptic terminals but no protection of neuronal dendrites. Only female IFNβ-deficient HIVgp120tg mice display diminished microglial activation in cortex and hippocampus and increased astrocytosis in hippocampus compared to their IFNβ-expressing counterparts. RNA expression for some immune genes and ISGs is also affected in a sex-dependent way. The IFNβKO abrogates or diminishes the induction of MX1, DDX58, IRF7 and IRF9 in HIVgp120tg brains of both sexes. Expression analysis of neurotransmission related genes reveals an influence of IFNβ on multiple components with more pronounced changes in IFNβKO females. In contrast, the effects of IFNβKO on MAPK activities are independent of sex with pronounced reduction of active ERK1/2 but also of active p38 in the HIVgp120tg brain. In summary, our findings show that the absence of IFNβ impairs memory dependent behavior and modulates neuropathology in HIVgp120tg brains, indicating that its absence may facilitate development of HAND. Moreover, our data suggests that endogenous IFNβ plays a vital role in maintaining neuronal homeostasis and memory function.
MeSH term(s)	Animals ; Female ; Male ; Mice ; Brain/metabolism ; HIV Infections/metabolism ; HIV-1/metabolism ; Interferon-beta/metabolism ; Mice, Transgenic
Chemical Substances	Interferon-beta (77238-31-4)
Language	English
Publishing date	2024-02-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2024.02.014
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 327: Show issues

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Book: Einführung in die Integrative Körperpsychotherapie IBP (Integrative Body Psychotherapy)

Kaul, Eva / Fischer, Markus

2016

Author's details	Eva Kaul und Markus Fischer
Keywords	Integrative Körperpsychotherapie
Language	German
Size	288 Seiten, Illustrationen, Diagramme, 24 cm x 17.5 cm
Edition	1. Auflage
Publisher	Hogrefe
Publishing place	Bern
Publishing country	Switzerland
Document type	Book
HBZ-ID	HT018991924
ISBN	978-3-456-85506-6 ; 9783456755069 ; 9783456955063 ; 3-456-85506-0 ; 3456755066 ; 3456955065
Database	Catalogue ZB MED Medicine, Health

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Shelf mark	Loan status	Location
2016 A 1312	available for loan (reading room)	Lesesaal EG

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Article ; Online: Publisher Correction: Mechanisms underlying HIV-associated cognitive impairment and emerging therapies for its management.

Ellis, Ronald J / Marquine, María J / Kaul, Marcus / Fields, Jerel Adam / Schlachetzki, Johannes C M

Nature reviews. Neurology

2023 Volume 19, Issue 12, Page(s) 787

Language	English
Publishing date	2023-10-11
Publishing country	England
Document type	Published Erratum
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-023-00895-y
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Zs.A 6257: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 88: Show issues

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Article ; Online: ACCT is a fast and accessible automatic cell counting tool using machine learning for 2D image segmentation.

Kataras, Theodore J / Jang, Tyler J / Koury, Jeffrey / Singh, Hina / Fok, Dominic / Kaul, Marcus

Scientific reports

2023 Volume 13, Issue 1, Page(s) 8213

Abstract: Counting cells is a cornerstone of tracking disease progression in neuroscience. A common approach for this process is having trained researchers individually select and count cells within an image, which is not only difficult to standardize but also ... ...

Abstract	Counting cells is a cornerstone of tracking disease progression in neuroscience. A common approach for this process is having trained researchers individually select and count cells within an image, which is not only difficult to standardize but also very time-consuming. While tools exist to automatically count cells in images, the accuracy and accessibility of such tools can be improved. Thus, we introduce a novel tool ACCT: Automatic Cell Counting with Trainable Weka Segmentation which allows for flexible automatic cell counting via object segmentation after user-driven training. ACCT is demonstrated with a comparative analysis of publicly available images of neurons and an in-house dataset of immunofluorescence-stained microglia cells. For comparison, both datasets were manually counted to demonstrate the applicability of ACCT as an accessible means to automatically quantify cells in a precise manner without the need for computing clusters or advanced data preparation.
MeSH term(s)	Image Processing, Computer-Assisted/methods ; Tool Use Behavior ; Machine Learning ; Cell Count/methods ; Neurons
Language	English
Publishing date	2023-05-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-34943-w
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Article ; Online: Mechanisms underlying HIV-associated cognitive impairment and emerging therapies for its management.

Ellis, Ronald J / Marquine, María J / Kaul, Marcus / Fields, Jerel Adam / Schlachetzki, Johannes C M

Nature reviews. Neurology

2023 Volume 19, Issue 11, Page(s) 668–687

Abstract: People living with HIV are affected by the chronic consequences of neurocognitive impairment (NCI) despite antiretroviral therapies that suppress viral replication, improve health and extend life. Furthermore, viral suppression does not eliminate the ... ...

Abstract	People living with HIV are affected by the chronic consequences of neurocognitive impairment (NCI) despite antiretroviral therapies that suppress viral replication, improve health and extend life. Furthermore, viral suppression does not eliminate the virus, and remaining infected cells may continue to produce viral proteins that trigger neurodegeneration. Comorbidities such as diabetes mellitus are likely to contribute substantially to CNS injury in people living with HIV, and some components of antiretroviral therapy exert undesirable side effects on the nervous system. No treatment for HIV-associated NCI has been approved by the European Medicines Agency or the US Food and Drug Administration. Historically, roadblocks to developing effective treatments have included a limited understanding of the pathophysiology of HIV-associated NCI and heterogeneity in its clinical manifestations. This heterogeneity might reflect multiple underlying causes that differ among individuals, rather than a single unifying neuropathogenesis. Despite these complexities, accelerating discoveries in HIV neuropathogenesis are yielding potentially druggable targets, including excessive immune activation, metabolic alterations culminating in mitochondrial dysfunction, dysregulation of metal ion homeostasis and lysosomal function, and microbiome alterations. In addition to drug treatments, we also highlight the importance of non-pharmacological interventions. By revisiting mechanisms implicated in NCI and potential interventions addressing these mechanisms, we hope to supply reasons for optimism in people living with HIV affected by NCI and their care providers.
MeSH term(s)	Humans ; HIV Infections/complications ; HIV Infections/drug therapy ; Central Nervous System Diseases ; Cognitive Dysfunction/etiology ; Cognitive Dysfunction/therapy
Language	English
Publishing date	2023-10-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2491514-2
ISSN	1759-4766 ; 1759-4758
ISSN (online)	1759-4766
ISSN	1759-4758
DOI	10.1038/s41582-023-00879-y
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Zs.MG 88: Show issues

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Article ; Online: Innate Immune Sensing of Viruses and Its Consequences for the Central Nervous System.

Singh, Hina / Koury, Jeffrey / Kaul, Marcus

Viruses

2021 Volume 13, Issue 2

Abstract: Viral infections remain a global public health concern and cause a severe societal and economic burden. At the organismal level, the innate immune system is essential for the detection of viruses and constitutes the first line of defense. Viral ... ...

Abstract	Viral infections remain a global public health concern and cause a severe societal and economic burden. At the organismal level, the innate immune system is essential for the detection of viruses and constitutes the first line of defense. Viral components are sensed by host pattern recognition receptors (PRRs). PRRs can be further classified based on their localization into Toll-like receptors (TLRs), C-type lectin receptors (CLR), retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), NOD-like receptors (NLRs) and cytosolic DNA sensors (CDS). TLR and RLR signaling results in production of type I interferons (IFNα and -β) and pro-inflammatory cytokines in a cell-specific manner, whereas NLR signaling leads to the production of interleukin-1 family proteins. On the other hand, CLRs are capable of sensing glycans present in viral pathogens, which can induce phagocytic, endocytic, antimicrobial, and pro- inflammatory responses. Peripheral immune sensing of viruses and the ensuing cytokine response can significantly affect the central nervous system (CNS). But viruses can also directly enter the CNS via a multitude of routes, such as the nasal epithelium, along nerve fibers connecting to the periphery and as cargo of infiltrating infected cells passing through the blood brain barrier, triggering innate immune sensing and cytokine responses directly in the CNS. Here, we review mechanisms of viral immune sensing and currently recognized consequences for the CNS of innate immune responses to viruses.
MeSH term(s)	Animals ; Central Nervous System/immunology ; Central Nervous System/virology ; Cytokines/metabolism ; Humans ; Immunity, Innate ; Inflammasomes ; Interferon Type I/metabolism ; Lectins, C-Type/metabolism ; Receptors, Pattern Recognition ; Signal Transduction ; Toll-Like Receptors/metabolism ; Virus Diseases/immunology
Chemical Substances	Cytokines ; Inflammasomes ; Interferon Type I ; Lectins, C-Type ; Receptors, Pattern Recognition ; Toll-Like Receptors
Language	English
Publishing date	2021-01-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v13020170
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Article ; Online: Beneficial and Adverse Effects of cART Affect Neurocognitive Function in HIV-1 Infection: Balancing Viral Suppression against Neuronal Stress and Injury.

Yuan, Nina Y / Kaul, Marcus

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2019 Volume 16, Issue 1, Page(s) 90–112

Abstract: HIV-associated neurocognitive disorders (HAND) persist despite the successful introduction of combination antiretroviral therapy (cART). While insufficient concentration of certain antiretrovirals (ARV) may lead to incomplete viral suppression in the ... ...

Abstract	HIV-associated neurocognitive disorders (HAND) persist despite the successful introduction of combination antiretroviral therapy (cART). While insufficient concentration of certain antiretrovirals (ARV) may lead to incomplete viral suppression in the brain, many ARVs are found to cause neuropsychiatric adverse effects, indicating their penetration into the central nervous system (CNS). Several lines of evidence suggest shared critical roles of oxidative and endoplasmic reticulum stress, compromised neuronal energy homeostasis, and autophagy in the promotion of neuronal dysfunction associated with both HIV-1 infection and long-term cART or ARV use. As the lifespans of HIV patients are increased, unique challenges have surfaced. Longer lives convey prolonged exposure of the CNS to viral toxins, neurotoxic ARVs, polypharmacy with prescribed or illicit drug use, and age-related diseases. All of these factors can contribute to increased risks for the development of neuropsychiatric conditions and cognitive impairment, which can significantly impact patient well-being, cART adherence, and overall health outcome. Strategies to increase the penetration of cART into the brain to lower viral toxicity may detrimentally increase ARV neurotoxicity and neuropsychiatric adverse effects. As clinicians attempt to control peripheral viremia in an aging population of HIV-infected patients, they must navigate an increasingly complex myriad of comorbidities, pharmacogenetics, drug-drug interactions, and psychiatric and cognitive dysfunction. Here we review in comparison to the neuropathological effects of HIV-1 the available information on neuropsychiatric adverse effects and neurotoxicity of clinically used ARV and cART. It appears altogether that future cART aiming at controlling HIV-1 in the CNS and preventing HAND will require an intricate balancing act of suppressing viral replication while minimizing neurotoxicity, impairment of neurocognition, and neuropsychiatric adverse effects. Graphical abstract Schematic summary of the effects exerted on the brain and neurocognitive function by HIV-1 infection, comorbidities, psychostimulatory, illicit drugs, therapeutic drugs, such as antiretrovirals, the resulting polypharmacy and aging, as well as the potential interactions of all these factors.
MeSH term(s)	AIDS Dementia Complex/drug therapy ; Anti-HIV Agents/adverse effects ; Anti-HIV Agents/pharmacology ; Anti-HIV Agents/therapeutic use ; Antiretroviral Therapy, Highly Active ; Comorbidity ; Drug Interactions ; HIV-1/drug effects ; HIV-1/pathogenicity ; Humans ; Illicit Drugs/pharmacokinetics ; Neurocognitive Disorders/chemically induced ; Neurocognitive Disorders/etiology ; Neurons/drug effects ; Neurons/virology ; Polypharmacy
Chemical Substances	Anti-HIV Agents ; Illicit Drugs
Language	English
Publishing date	2019-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-019-09868-9
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