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Biomedicines
Special Issues
Immune Landscape in Neurodegenerative Diseases
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Immune Landscape in Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 10258

Special Issue Editors

Prof. Dr. Frederico Pereira

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Guest Editor
Institute of Pharmacology and Experimental Therapeutics/Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Subunit 1–Pólo 3, Azinhaga de Santa Comba, Celas, 3000-354 Coimbra, Portugal
Interests: neuropsychopharmacology; neuroimmunology; brain diseases; physical exercise; drugs of abuse
Dr. Cristoforo Comi

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Guest Editor
Department of Translational Medicine, Section of Neurology, University of Piemonte Orientale, 28100 Novara, Italy
Interests: neurodegenerative diseases including Parkinson’s disease; Huntington’s disease; other movement disorders; Alzheimer’s disease; neuroimmune diseases including: multiple sclerosis, inflammatory neuropathies, myasthenia gravis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Marco Cosentino

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Guest Editor
Center for Research in Medical Pharmacology, University of Insubria, 21100 Varese, Italy
Interests: neuroimmune pharmacology; clinical pharmacology; pharmacogenetics; herbal medicine

Special Issue Information

Dear Colleagues,

Neuroinflammation is a standing out feature and a likely contributor to neurodegenerative diseases, such as Alzheimer’s disease and other dementias, Parkinson’s disease, Huntington disease, amyotrophic lateral sclerosis, among others. Native central nervous system (CNS) cells, comprising microglia (major immune functions include cytokine production, phagocytosis), astrocytes [major immune functions include blood brain barrier (BBB)  maintenance, cytokine secretion, glial scar formation], ependydimal cells (major immune functions include the blood-cerebrospinal fluid (CSF) barrier (BCSFB) maintenance, pathogen surveillance, inflammatory signaling) and neurons [major immune functions include inflammatory signaling via citokynes, damage associated molecular patterns (DAMPS) and neurotransmitters/peptides] play key roles in neuroinflammation. Specifically, microglia/astrocytes have received significant attention as therapeutic targets. Importantly, there is a growing body of evidence implying peripheral immune cells, including neutrophils, basophils, monocytes, dendritic cells, Natural Killer (NK) cells and T cells,  in neuroinflammation processes underlying neurodegenerative disorders. Particularly, the central-peripheral immune crosstalk is an active area of research aiming to provide new disease-modifying strategies which remain an unmet need in this context.

Prof. Dr. Frederico Pereira
Prof. Dr. Cristoforo Comi
Prof. Dr. Marco Cosentino
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • neurodegenerative disorders
  • neuroinflammation
  • central and peripheral immune system
  • microglia
  • astrocytes
  • ependydimal cells
  • BBB
  • BCSFB
  • DAMPs
  • mast cells
  • neutrophils
  • basophils
  • monocytes
  • macrophages
  • dendritic cells
  • NK cells
  • T cells

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Published Papers (2 papers)

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14 pages, 758 KiB  
Article
Systemic Inflammation Predicts Alzheimer Pathology in Community Samples without Dementia
by Nicolas Cherbuin, Erin I. Walsh, Liana Leach, Anne Brüstle, Richard Burns, Kaarin J. Anstey, Perminder S. Sachdev and Bernhard T. Baune
Biomedicines 2022, 10(6), 1240; https://doi.org/10.3390/biomedicines10061240 - 26 May 2022
Cited by 8 | Viewed by 3088
Abstract
Neuroinflammation and oxidative stress (OS) are implicated in the pathophysiology of Alzheimer’s disease (AD). However, it is unclear at what stage of the disease process inflammation first becomes manifest. The aim of this study was to investigate the associations between specific plasma markers [...] Read more.
Neuroinflammation and oxidative stress (OS) are implicated in the pathophysiology of Alzheimer’s disease (AD). However, it is unclear at what stage of the disease process inflammation first becomes manifest. The aim of this study was to investigate the associations between specific plasma markers of inflammation and OS, tau, and Amyloid-β 38, 40, and 42 levels in cognitively unimpaired middle-age and older individuals. Associations between inflammatory states identified through principal component analysis and AD biomarkers were investigated in middle-age (52–56 years, n = 335, 52% female) and older-age (72–76 years, n = 351, 46% female) participants without dementia. In middle-age, a component reflecting variation in OS was most strongly associated with tau and to a lesser extent amyloid-β levels. In older-age, a similar component to that observed in middle-age was only associated with tau, while another component reflecting heightened inflammation independent of OS, was associated with all AD biomarkers. In middle and older-age, inflammation and OS states are associated with plasma AD biomarkers. Full article
(This article belongs to the Special Issue Immune Landscape in Neurodegenerative Diseases)
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Review

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27 pages, 5266 KiB  
Review
The Forgotten Brother: The Innate-like B1 Cell in Multiple Sclerosis
by Saar T. Halperin, Bert A. ’t Hart, Antonio Luchicchi and Geert J. Schenk
Biomedicines 2022, 10(3), 606; https://doi.org/10.3390/biomedicines10030606 - 4 Mar 2022
Cited by 7 | Viewed by 6116
Abstract
Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS), traditionally considered a chronic autoimmune attack against the insulating myelin sheaths around axons. However, the exact etiology has not been identified and is likely multi-factorial. Recently, evidence has been accumulating [...] Read more.
Multiple sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS), traditionally considered a chronic autoimmune attack against the insulating myelin sheaths around axons. However, the exact etiology has not been identified and is likely multi-factorial. Recently, evidence has been accumulating that implies that autoimmune processes underlying MS may, in fact, be triggered by pathological processes initiated within the CNS. This review focuses on a relatively unexplored immune cell—the “innate-like” B1 lymphocyte. The B1 cell is a primary-natural-antibody- and anti-inflammatory-cytokine-producing cell present in the healthy brain. It has been recently shown that its frequency and function may differ between MS patients and healthy controls, but its exact involvement in the MS pathogenic process remains obscure. In this review, we propose that this enigmatic cell may play a more prominent role in MS pathology than ever imagined. We aim to shed light on the human B1 cell in health and disease, and how dysregulation in its delicate homeostatic role could impact MS. Furthermore, novel therapeutic avenues to restore B1 cells’ beneficial functions will be proposed. Full article
(This article belongs to the Special Issue Immune Landscape in Neurodegenerative Diseases)
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