journal: NeuroImmune Pharmacology and Therapeutics

Open Access Published since May 20, 2022

NeuroImmune Pharmacology and Therapeutics

ISSN: 2750-6665

Editor-in-chief: Howard E. Gendelman

Submit manuscript

About this journal

Objective

NeuroImmune Pharmacology and Therapeutics is the official peer-reviewed journal of the Society on NeuroImmune Pharmacology. Owned by the Society, the open-access journal showcases cutting-edge research in four core areas: neuroscience, immunology, pharmacology, and therapeutics. Published manuscripts focus on any one of these subject areas and/or their intersections to advance basic, clinical, and translational science.

Specific aims:

To promote diverse neuroimmune research activities in molecular, biochemical, genetic, and pathogenetic studies that advance pharmacologic and therapeutic scholarship.

To present cutting-edge laboratory, translational, and clinical research on substance use disorders (biology, pathophysiology, behavior, and structure-function relationships) and neurodegenerative, neuroinfectious, metabolic, inflammatory, behavioral, and infectious diseases.

To present therapeutic works with molecular, structural-surgical (interventions), and biochemical approaches that serve to ameliorate, delay, or arrest disease onset and/or progression.

To present new, highly interactive, and cross-disciplinary research that intersects the fields of drug delivery, neuroscience, and immunology relevant to modulating or transforming the neuroimmune axis.

To provide a platform for divergent and prospective points of view, letters, and/or brief communications on recent topics of immediate interest.

To foster immediate/relevant information exchanges for neuroimmune therapeutics, disease prevention and treatment strategies in support of topical supplementary reviews with interactions and/or support of the views and directions of the Society on Neuroimmune Pharmacology.

To support and encourage scientific exchange between Society members, authors in or outside the field of neuroimmune therapeutics, and reaching into an international field of investigators that span the globe.

To promote scholarly submissions on the etiology, prevention, and treatment of neuroimmune disorders (including clinical trials) where therapeutic intervention has proven viable and active.

To define the neuroimmunomodulator properties of neuroimmune innervations and regeneration, and of endogenous and exogenous neuroimmunomodulator substances, that would include (but are not limited to) hormones, neuropeptides, neurotransmitters, cytokines, chemokines, and abused substances.

To advance actively developing fields of research in neuroimmune pharmacology (including but not limited to nano-medicine, therapeutics, technology, and gene editing).

To promote translational research in general and, in particular, a better understanding of the role played by neuroinfectious diseases, inflammation, and stress in disorders of the neuroimmune axis.

The overarching scope of the journal is to provide a platform for promoting the Society’s research and to extend that vision on a global scale in basic, clinical, and translational science.

Abstracting and Indexing

NeuroImmune Pharmacology and Therapeutics is covered by the following services:

Baidu Scholar
CNKI Scholar (China National Knowledge Infrastructure)
CNPIEC - cnpLINKer
Dimensions
EBSCO Discovery Service
Google Scholar
J-Gate
JournalTOCs
KESLI-NDSL (Korean National Discovery for Science Leaders)
MyScienceWork
Naver Academic
Naviga (Softweco)
Primo Central (ExLibris)
ReadCube
Scilit
Semantic Scholar
Summon (ProQuest)
TDNet
WorldCat (OCLC)
X-MOL
Yewno Discover

Supplementary Materials

Topics

External Links

Online Submission of Manuscripts

Volume 2 Issue 3

September 2023

Publicly Available September 4, 2023

Frontmatter

Page range: i-iii

Download PDF

Brief Report

Open Access June 26, 2023

NLRP3 inflammasome activation underlies the neuro-oxidative stress associated with Methamphetamine (METH) and SARS-CoV2 induced co-morbidity in human microglia

Janvhi Suresh Machhar, Elias Abou-Jaoude, Stanley A. Schwartz, Ravikumar Aalinkeel, Supriya D. Mahajan

Page range: 245-252

More Download PDF

Abstract

Acute and chronic use of Methamphetamine (METH) has critical immunological implications and METH users are more vulnerable to SARS-CoV2 infection. Inflammasomes are activated in response to SARS-CoV2 infection. METH also activates NLRP3 inflammasome in microglia and promotes neuro cognitive deficits. The goal of the study was to examine the involvement of NLRP3 inflammasome in METH and/or SARS-CoV2 induced neuro-oxidative stress in microglial cells. Our results suggests that METH +/− SARS-CoV2 initiated a neuro immune-inflammatory response and mitochondrial oxidative stress via NLRP3 inflammasome activation induced increased Caspase −1 and increased lipid peroxidation. Our data suggests that SARS-CoV2 infection in METH abusing subjects may result in long-term neurological deficits resulting from microglial dysfunction and apoptosis attributed to NLRP3 inflammasome activation.

Review Article

Open Access July 10, 2023

The elusive role of herpesviruses in Alzheimer’s disease: current evidence and future directions

Stacey L. Piotrowski, Allison Tucker, Steven Jacobson

Page range: 253-266

More Download PDF

Abstract

Alzheimer’s disease (AD) is the most common cause of dementia. While pathologic hallmarks, such as extracellular beta-amyloid plaques, are well-characterized in affected individuals, the pathogenesis that causes plaque formation and eventual cognitive decline is not well understood. A recent resurgence of the decades-old “infectious hypothesis” has garnered increased attention on the potential role that microbes may play in AD. In this theory, it is thought that pathogens such as viruses may act as seeds for beta-amyloid aggregation, ultimately leading to plaques. Interest in the infectious hypothesis has also spurred further investigation into additional characteristics of viral infection that may play a role in AD progression, such as neuroinflammation, latency, and viral DNA integration. While a flurry of research in this area has been recently published, with herpesviruses being of particular interest, the role of pathogens in AD remains controversial. In this review, the insights gained thus far into the possible role of herpesviruses in AD are summarized. The challenges and potential future directions of herpesvirus research in AD and dementia are also discussed.

Research Articles

Open Access February 21, 2023

Network meta-analysis on alcohol-mediated modulation of Alzheimer’s disease in the diseases of inflammation including COVID-19

Muhammed Bishir, Tatiana Rengifo, Wenfei Huang, Ryan J. Kim, Saravana Babu Chidambaram, Sulie L. Chang

Page range: 267-281

More Download PDF

Abstract

Objectives Cross sectional surveys have reported that alcohol consumption has skyrocketed during the COVID-19 pandemic. Chronic alcohol use triggers systemic inflammation which leads to neuroinflammation and neurodegeneration. In the present study, we hypothesize that alcohol consumption and cytokine elevation during inflammatory conditions synergistically increase amyloid-beta precursor protein (APP) expression and worsens Alzheimer’s disease (AD) pathology. Methods QIAGEN Ingenuity Pathway Analysis (IPA) was employed to conduct network meta-analysis on the molecular mechanisms underlying ethanol (EtOH) influence on APP expression and AD in inflammatory conditions including COVID-19, inflammation of respiratory system, organ, absolute anatomical region, body cavity, joint, respiratory system component, gastrointestinal tract, large intestine, liver, central nerve system, and lung. IPA tools were utilized to identify the molecules associated with EtOH, inflammatory conditions and the common molecules between them. Results Simulation activity of EtOH, mimicking exposure to alcohol, upregulated the APP expression and augmented AD pathology in all inflammatory conditions including COVID-19. Our studies identified six molecules including ADORA2A, Cytokine, IFN-gamma, IL1-beta, Immunoglobulin and TNF, which concurrently contribute to increased APP expression and AD progression upon EtOH simulation in all diseases studied. Conclusions The present study has revealed molecular mechanisms underlying alcohol augmentation of AD in COVID-19 and other diseases of inflammation.

Open Access August 4, 2022

Meta-analysis of the effects of palmitic acid on microglia activation and neurodegeneration

Heping Zhou, Sulie L. Chang

Page range: 281-291

More Download PDF

Abstract

Objectives Evidence suggests that obesity may represent a risk factor for neurodegenerative pathologies including Alzheimer’s disease (AD). With excessive accumulation of adipose tissue, obesity is associated with chronic low-grade inflammation, increased production of adipokines, elevated levels of free fatty acids (FFAs) including palmitic acid (PA), the most abundant saturated fatty acid (SFA) in circulation. Excessive PA has been shown to induce lipotoxicity in many different types of cells including microglia and neuronal cells. We hypothesized that PA may contribute to the development of obesity-associated neurological conditions. Methods This study was designed to examine how increased PA may affect microglia activation and neurodegeneration using QIAGEN Ingenuity Pathway Analysis (IPA). Kramer analysis was used to quantitatively characterize the impact of PA on microglia activation and neurodegeneration. Results Simulated increase of PA enhanced the activities of intermediating molecules including CCL5, IL1β, IL1RN, IL6, NF-κB, NOS2, PTGS2, TLR2, TLR4, and TNF. Increased PA level induced microglia activation with a z score of 2.38 (p=0.0173) and neurodegeneration with a z score of 1.55 (p=0.121). Increased PA level also activated neuroinflammation signaling pathway, the top canonical pathway associated with both microglia activation and neurodegeneration. Conclusions Our IPA analysis demonstrated that increased PA significantly induced microglia activation and might augment neurodegeneration by altering the activities of key intermediating molecules and canonical pathways. Our findings shed light on how increased PA level may contribute to the development of neurodegenerative pathologies in the course of obesity.

Open Access August 2, 2023

A simple protocol for isolating microglia from adult mouse brain

Sudipta Chakrabarti, Sukhamoy Gorai, Kalipada Pahan

Page range: 293-300

More Download PDF

Abstract

Objectives Although microglia are activated in adult and aged brains resulting in neurodegenerative and neuroinflammatory disorders, most of the cell culture studies on microglia deal with neonatal microglia because of ease of isolation. Microglia could be isolated from adult brains, but it requires separation by density gradient centrifugation, magnetic beads, etc. Here, we describe a simple protocol of isolating highly purified microglia from adult mouse brains. Methods Our protocol involves dilution with sterile PBS or media, regular centrifugation, and plating on poly-D-lysine-coated flasks. Results These adult microglia expressed the inducible nitric oxide synthase in response to preformed α-syn fibril, an etiological reagent of Parkinson’s disease, and bacterial lipopolysaccharides, one of the prototype proinflammatory stimuli. Moreover, these adult microglia exhibited phagocytosis, which was stimulated by LPS treatment. Conclusions These results suggest that adult microglia isolated by our procedure are functional and that these adult microglia could be used for studies related to neurodegenerative disorders.

Review Article

Open Access July 31, 2023

Substances of abuse and their effect on SAR-CoV-2 pathogenesis

Ivy Antwi, Destiny Watkins, Alahn Pedawi, Atheel Ghrayeb, Christine Van de Vuurst, Theodore J. Cory

Page range: 301-316

More Download PDF

Abstract

Following the emergence of SARS-CoV-2, various reports suggest that there has been a significant increase in substance abuse due to social distancing and related issues. Several reports have suggested the impact of chronic substance use on individuals’ physiological and psychological health. Therefore, there is a need to know the impact of SARS-CoV-2 on persons with substance use disorders. Individuals with substance use disorders are the most vulnerable groups and are at a high risk of SARS-CoV-2 infection due to their already existing health issues associated with substance use. This review discusses some of the molecular and systemic/organic effects chronic substance use such as alcohol, nicotine, marijuana (cannabis), opioids, methamphetamine, and cocaine have on SARS-CoV-2 infectivity and its potential cause for worsened disease outcomes in persons with substance use disorder. This will provide healthcare providers, public health policies, and researchers with the needed knowledge to address some of the many challenges faced during the Covid-19 pandemic to facilitate treatment strategies for persons with substance use disorders.

Research Article

Open Access August 14, 2023

Immune senescence in aged APP/PS1 mice

Mai M. Abdelmoaty, Pravin Yeapuri, Jatin Machhi, Yaman Lu, Krista L. Namminga, Rana Kadry, Eugene Lu, Shaurav Bhattarai, Rodney Lee Mosley, Howard E. Gendelman

Page range: 317-330

More Download PDF

Abstract

Objectives To evaluate the linkage between age and deficits in innate and adaptive immunity which heralds both Alzheimer’s disease (AD) onset and progression. The pathobiological events which underlie and tie these outcomes remain not fully understood. Methods To investigate age-dependent immunity in AD, we evaluated innate and adaptive immunity in coordinate studies of regulatory T cell (Treg) function, T cell frequencies, and microglial integrity. These were assessed in blood, peripheral lymphoid tissues, and the hippocampus of transgenic (Tg) amyloid precursor protein/presenilin 1 (APP/PS1) against non-Tg mice. Additionally, immune arrays of hippocampal tissue were performed at 4, 6, 12, and 20 months of age. Results APP/PS1 mice showed progressive impairment of Treg immunosuppressive function with age. There was partial restoration of Treg function in 20-month-old mice. Ingenuity pathway analyses of hippocampal tissues were enriched in inflammatory, oxidative, and cellular activation pathways that paralleled advancing age and AD-pathobiology. Operative genes in those pathways included, but were not limited to triggering receptor on myeloid cells 1 (TREM1), T helper type 1 (Th1), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways. Interleukin-17 (IL-17), nitric oxide, acute phase, and T cell receptor signaling pathways were also perturbed. Significant inflammation was observed at 6- and 12-months. However, at 20-months, age associated partial restoration of Treg function reduced inflammatory phenotype. Conclusions Impaired Treg function, inflammation and oxidative stress were associated with AD pathology. Age associated partial restoration of Treg function in old mice reduced the hippocampal inflammatory phenotype. Restoring Treg suppressive function can be a therapeutic modality for AD.

Ahead of Print / Just Accepted

Ahead of Print / Just Accepted

Volume 2 (2023)

Volume 1 (2022)

Issue 1

No ranking information is available for this journal.

Submit

Submission
You can easily submit your manuscript online. Simply go to http://mc.manuscriptcentral.com/nipt and you will be guided through the whole submission and publishing process.

Additionally, the Template for Ethical and Legal Declarations needs to be customized by the submitting author on behalf of all others and uploaded as a separate doc-file at the time of the original submission. Instructions on how to make declarations can be found here.

Your benefits of publishing with us

Open Access publication
Research freely available for all to read and download
Authors retain copyright – articles published under the Creative Commons Attribution (CC-BY-4.0) License
Rapid publication times
Free publication of color figures
Every article easily discoverable because of Search Engine Optimization (SEO) and comprehensive abstracting and indexing services
Professional sales and marketing activities

Submission process

Submission of your manuscript via our submission management tool following the Information for Authors
Single-blind peer review process
A decision on your paper is aspired within 4-5 weeks
Accepted articles are published online approx. 3 weeks after acceptance

Please note

Publication language is English. Manuscripts must be written in clear and concise English
The Template for Ethical and Legal Declarations are required for submission
If you have any general questions please visit our FAQ for authors
For more detailed information please contact the NIPT Editorial Office nipt@unmc.edu

We are looking forward to receiving your manuscript!

Editorial

Editor-in-Chief
Howard E. Gendelman, M.D.
Department of Pharmacology and Experimental Neuroscience
University of Nebraska Medical Center
Omaha, NE, USA

Managing Editor
Amy Sather
University of Nebraska Medical Center
Omaha, NE, USA
Contact: nipt@unmc.edu

Editors

Senior Editor (North America)
Kalipada Pahan, Ph.D.
Department of Neurological Sciences
Rush University Medical Center
Chicago, IL, USA

Senior Editor (Asia and Pacific Rim)
Raymond Chuen-Chung Chang, Ph.D.
School of Biomedical Sciences
The University of Hong Kong
Hong Kong, China

Senior Editor (Europe)
Marco Cosentino, M.D., Ph.D.
Department of Medicine and Surgery
University of Insubria
Varese, Lombardy, Italy

Section Editor (Neuroactive and Abused Substances)
Sabita Roy, Ph.D.
Departments of Surgery, Microbiology and Immunology, and Biochemistry
University of Miami Miller School of Medicine
Miami, FL, USA

Section Editor (Imaging and Biomarkers)
Linda Chang, M.D., M.S.
Departments of Diagnostic Radiology and Nuclear Medicine, and Neurology
University of Maryland School of Medicine
Department of Neurology, Johns Hopkins School of Medicine
Baltimore, MD, USA

Section Editor (Neurotherapeutics)
Harris A. Gelbard, M.D., Ph.D.
Department of Neurology
University of Rochester Medical Center
Rochester, NY, USA

Section Editor (Neurodegenerative Disorders)
Tsuneya Ikezu, M.D., Ph.D.
Department of Neuroscience
Mayo Clinic Florida
Jacksonville, FL, USA

Section Editor (Neuroimmunology)
Steven Jacobson, Ph.D.
Viral Immunology Section
National Institute of Neurological Disorders and Stroke
Bethesda, MD, USA

Section Editor (Nanomedicine)
Ram I. Mahato, Ph.D.
Department of Pharmaceutical Sciences
University of Nebraska Medical Center
Omaha, NE, USA

Section Editor (Cell Signaling and Immunity)
Thomas J. Rogers, Ph.D.
Center for Inflammation and Lung Research
Lewis Katz School of Medicine of Temple University
Philadelphia, PA, USA

Section Editor (Immunopharmacology)
Eliseo Eugenin, M.D., Ph.D.
Department of Neuroscience
University of Texas Medical Branch
Austin, TX, USA

Section Editor (Inflammatory Transformation)
Stanley H. Appel, M.D.
Houston Methodist Neurological Institute
Houston Methodist
Houston, TX, USA

Section Editor (Medicinal Chemistry)
Corey R. Hopkins, Ph.D.
Pharmaceutical Sciences
University of Nebraska Medical Center
Omaha, NE, USA

Section Editor (Material Science and Drug Delivery)
Dan Peer, Ph.D.
Laboratory of Precision NanoMedicine
Tel Aviv University
Tel Aviv, Israel

Section Editor (Infectious Disease)
Vicente Soriano, M.D., Ph.D.
Health Sciences School and Medical Center
International University of La Rioja
Madrid, Spain

Editorial Board

Chandravanu Dash, Ph.D.
Vanderbilt Institute for Infection, Immunology and Inflammation
Vanderbilt University Medical Center
Nashville, TN USA

Siddappa Byrareddy, Ph.D.
Department of Pharmacology & Experimental Neuroscience
University of Nebraska Medical Center
Omaha, NE USA

Pooja Jain, Ph.D.
Microbiology & Immunology
Drexel University College of Medicine
Philadelphia, PA USA

Toby Eisenstein, Ph.D.
Center for Substance Abuse and Research
Lewis Katz School of Medicine
Philadelphia, PA USA

Olimpia Meucci, M.D., Ph.D.
Pharmacology & Physiology
Drexel School of Medicine
Philadelphia, PA USA

Dionna Williams, Ph.D.
Molecular and Comparative Pathobiology
Johns Hopkins Medicine
Baltimore, MD USA

Yuri Persidsky, M.D., Ph.D.
Department of Pathology and Laboratory Medicine
Lewis Katz School of Medicine
Philadelphia, PA USA

Larisa Poluektova, M.D., Ph.D.
Department of Pharmacology & Experimental Neuroscience
University of Nebraska Medicine
Omaha, NE USA

Ronald Ellis, M.D., Ph.D.
Neuroscience and Psychiatry
University of California, San Diego
San Diego, CA USA

Johnny He, Ph.D.
Department of Immunology and Infection
Rosalind Franklin University of Medicine and Science
North Chicago, IL USA

Nazira El-Hage, Ph.D.
Department of Immunology & Nano-Medicine
Florida International University
Miami, FL USA

Shilpa Buch, Ph.D.
Department of Pharmacology & Experimental Neuroscience
University of Nebraska Medical Center
Omaha, NE USA

Wenzhe Ho, M.D., MPH
Department of Pathology and Laboratory Medicine
Lewi Katz School of Medicine
Philadelphia, PA USA

Natalie May Zahr, Ph.D.
Department of Psychiatry and Behavioral Sciences
Stanford University School of Medicine
Stanford, CA USA

Advisory Board

Sulie L. Chang, Ph.D. ^*Institute of NeuroImmune Pharmacology and Department of Biological Sciences
Seton Hall University
South Orange, NJ, USA

Santosh Kumar, Ph.D. ^*Department of Pharmaceutical Sciences
College of Pharmacy
University of Tennessee Health Science Center Memphis
Memphis, TN, USA

Jean M. Bidlack, Ph.D. ^*Department of Pharmacology and Physiology
University of Rochester Medical Center
Rochester, NY, USA

Sanjay B. Maggirwar, Ph.D., M.B.A. ^*Department of Microbiology, Immunology, and Tropical Medicine
The George Washington University
Washington, D.C., USA

Carol J. Swarts, M.D. ^**University of Nebraska Medical Center
Seattle, WA, USA

Robert M. Eisenberg, J.D., M.A. ^**
Omaha, NE, USA

* Members of the Journal Publishing Committee of the Society on NeuroImmune Pharmacology.
** Major philanthropic supporters of the journal, NeuroImmune Pharmacology and Therapeutics.

(Deutsch)

Type: Journal
Language: English
Publisher: De Gruyter
First published: May 20, 2022
Publication Frequency: 4 Issues per Year