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Inflammation and Neurodegeneration
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Inflammation and Neurodegeneration

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 12118

Special Issue Editor

Dr. Douglas Gordon Walker

E-Mail Website
Guest Editor
School of Life Sciences and Neurodegenerative Disease Research Center, Arizona State University, Tempe, AZ, USA
Interests: human microglia; CD200; CD33; TREM-2; progranulin; autophagy; lysosomal function; amyloid beta; alpha synuclein; anti-inflammatory signaling; microglia phenotyping
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

There has recently been a paradigm shift in our consideration of how neuroinflammation might be involved in promoting the degenerative changes occurring in aging, Alzheimer’s disease (AD), and Parkinson’s disease (PD) brains. Recent gene expression profiling of microglia from human tissues and animal models has established that “disease-associated microglia” might be functioning to prevent inflammatory damage and not promote it. The inhibition of microglial inflammation has been associated with the reduced phagocytosis of toxic proteins (e.g., amyloid beta or tau). In addition, some of the single-nucleotide polymorphisms for altering disease risk located in genes with anti-inflammatory functions (CD33 and progranulin) and phagocytic functions (CD33 and triggering receptor expressed on myeloid cells (TREM-2)).  The general lack of effectiveness of immune therapy in ameliorating disease symptoms of AD has also raised issues about determining effective targets. There has also been renewed interest in and data on non-prescription/nutraceuticals such as caffeine, vitamin D, and curcumin as immune-modulating agents for treating these diseases. It is the goal of this Special Issue entitled “Inflammation and Neurodegeneration” to provide a forum to present new and revisited molecular and pharmaceutical targets that affect the interaction of microglia and astrocytes with the pathological features of these diseases. This Special Issue is seeking original research articles and reviews that address and challenge the current concepts of neuroinflammation in these uniquely human diseases. We welcome manuscripts detailing new and innovative models and agents, along with human-neuropathology-focused studies that investigate under-researched targets.

Dr. Douglas Gordon Walker
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • microglia
  • astrocytes
  • genetic risk factors
  • immune modulators
  • research models
  • phagocytosis
  • anti-inflammatory
  • disease pathways

Published Papers (2 papers)

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Review

24 pages, 7243 KiB  
Review
Thioredoxin-Interacting Protein (TXNIP) with Focus on Brain and Neurodegenerative Diseases
by Haruka Tsubaki, Ikuo Tooyama and Douglas Gordon Walker
Int. J. Mol. Sci. 2020, 21(24), 9357; https://doi.org/10.3390/ijms21249357 - 8 Dec 2020
Cited by 75 | Viewed by 8740
Abstract
The development of new therapeutic approaches to diseases relies on the identification of key molecular targets involved in amplifying disease processes. One such molecule is thioredoxin-interacting protein (TXNIP), also designated thioredoxin-binding protein-2 (TBP-2), a member of the α-arrestin family of proteins and a [...] Read more.
The development of new therapeutic approaches to diseases relies on the identification of key molecular targets involved in amplifying disease processes. One such molecule is thioredoxin-interacting protein (TXNIP), also designated thioredoxin-binding protein-2 (TBP-2), a member of the α-arrestin family of proteins and a central regulator of glucose and lipid metabolism, involved in diabetes-associated vascular endothelial dysfunction and inflammation. TXNIP sequesters reduced thioredoxin (TRX), inhibiting its function, resulting in increased oxidative stress. Many different cellular stress factors regulate TXNIP expression, including high glucose, endoplasmic reticulum stress, free radicals, hypoxia, nitric oxide, insulin, and adenosine-containing molecules. TXNIP is also directly involved in inflammatory activation through its interaction with the nucleotide-binding domain, leucine-rich-containing family, and pyrin domain-containing-3 (NLRP3) inflammasome complex. Neurodegenerative diseases such as Alzheimer’s disease have significant pathologies associated with increased oxidative stress, inflammation, and vascular dysfunctions. In addition, as dysfunctions in glucose and cellular metabolism have been associated with such brain diseases, a role for TXNIP in neurodegeneration has actively been investigated. In this review, we will focus on the current state of the understanding of possible normal and pathological functions of TXNIP in the central nervous system from studies of in vitro neural cells and the brains of humans and experimental animals with reference to other studies. As TXNIP can be expressed by neurons, microglia, astrocytes, and endothelial cells, a complex pattern of regulation and function in the brain is suggested. We will examine data suggesting TXNIP as a therapeutic target for neurodegenerative diseases where further research is needed. Full article
(This article belongs to the Special Issue Inflammation and Neurodegeneration)
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Graphical abstract

16 pages, 584 KiB  
Review
Glia in Neurodegeneration: The Housekeeper, the Defender and the Perpetrator
by Carrie Sheeler, Juao-Guilherme Rosa, Austin Ferro, Brian McAdams, Ella Borgenheimer and Marija Cvetanovic
Int. J. Mol. Sci. 2020, 21(23), 9188; https://doi.org/10.3390/ijms21239188 - 2 Dec 2020
Cited by 29 | Viewed by 2949
Abstract
Over the past decade, research has unveiled the intimate relationship between neuroinflammation and neurodegeneration. Microglia and astrocytes react to brain insult by setting up a multimodal inflammatory state and act as the primary defenders and executioners of neuroinflammatory structural and functional changes. Microglia [...] Read more.
Over the past decade, research has unveiled the intimate relationship between neuroinflammation and neurodegeneration. Microglia and astrocytes react to brain insult by setting up a multimodal inflammatory state and act as the primary defenders and executioners of neuroinflammatory structural and functional changes. Microglia and astrocytes also play critical roles in the maintenance of normal brain function. This intricate balance of homeostatic and neuroinflammatory functions can influence the onset and the course of neurodegenerative diseases. The emergent role of the microglial-astrocytic axis in neurodegenerative disease presents many druggable targets that may have broad therapeutic benefits across neurodegenerative disease. Here, we provide a brief review of the basal function of both microglia and astrocytes, how they are changed in disease states, the significant differences between mouse and human glia, and use of human induced pluripotent stem cells derived from patients to study cell autonomous changes in human astrocytes and microglia. Full article
(This article belongs to the Special Issue Inflammation and Neurodegeneration)
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