Skip to main content

Call for Papers - Neuroinflammation and Brain Disease

Guest Editors:
Anna Bersano: Istituto Neurologico "Carlo Besta", Italy
Jürgen Engele: University of Leipzig, Germany
Michael Schäfer: University Medical Center of Johannes Gutenberg University of Mainz, Germany 

Submission Status: Open   |   Submission Deadline: 31 July 2023


BMC Neurology and BMC Neuroscience are calling for submissions to our Collection on Neuroinflammation and Brain Disease.  Pathogenic conditions can trigger neuroinflammation leading to disruption of CNS structure and function. Neuroinflammation has a key role in the onset and/or progression of several CNS disorders, including acute brain injuries such as stroke and traumatic brain injury (TBI), and chronic neurodegenerative diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), Multiple sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). Additionally, with the advent of COVID-19, neuroinflammation in response to viral infections has received tremendous attention. The purpose of this collection is to provide the most up-to-date experimental and clinical research on key molecular pathways involved in neuroinflammation including research on therapeutic approaches and biomarkers.


Submit to collection

BMC Neurology

BMC Neuroscience

Meet the Guest Editors

Back to top

Anna Bersano: Istituto Neurologico "Carlo Besta", Italy

Dr. Anna Bersano is a Vascular neurologist, head of the cerebrovascular Unit at Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy. She has a long term expertise in Cerebrovascular disease and particularly heritable and rare causes of stroke as CADASIL, Moyamoya Disease, Fabry disease and Cerebral Amyloid Angiopathy (CAA).

 

Jürgen Engele: University of Leipzig, Germany

Prof. Engele received his PhD in human biology from the University of Ulm, Germany, followed by postdoctoral training at the Department of Neurobiology and Anatomy, University of Rochester, NY, USA. Since 2001 he is a professor of anatomy at the University of Leipzig, Germany. His long-standing research interest is the role of astrocytes in the healthy and diseased CNS. An additional focus of his research in recent years is the function of the CXCL12 receptor, CXCR7, in different types of cells and pathologies. 

Michael Schäfer: University Medical Center of Johannes Gutenberg University of Mainz, Germany

Michael Schäfer is a University Professor at the University Medical Center of the Johannes Gutenberg-University of Mainz, Germany since 2013. Michael investigates the pathological mechanisms of neurological disorders with a special focus on experimental brain injuries such as traumatic brain injury and stroke. He became a senior Editorial Board Member of BMC Neuroscience in 2020.

About the collection

BMC Neurology and BMC Neuroscience are calling for submissions to our Collection on Neuroinflammation and Brain Disease.  Inflammation is a biological process that dynamically alters the surrounding microenvironment, including participating immune cells. As a well-protected organ surrounded by specialized barriers and with immune privilege properties, the central nervous system (CNS) tightly regulates immune responses. In neuroinflammatory conditions, pathogenic immunity can disrupt CNS structure and function. Neuroinflammation has a key role in the onset and/or progression of several neurological disorders, including stroke, Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's condition, Multi-sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). 

Microglia are critical cells involved in the brain inflammation and specifically in inflammatory neurodegenerative diseases. Under the influence of exogenous and endogenous factors (trauma, stroke, chronic infections, disease related proteins like Aβ, Tau/p-Tau or α-syn,), the activation of microglia triggers several signal transduction pathways, including phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR), leading to NF-κB activation. The subsequent production of pro-inflammatory cytokines, chemokines, inducible enzymes (e.g., iNOS) and COX-2 drives to neuroinflammation.

Numerous studies have indeed documented the increased production of different cytokines including interleukin-1β (IL-1β), IL-6, IL-18, IL-12, IL-23, IL-33 and tumor necrosis factor-α (TNF-α) in various neurological and neuropsychiatric disorders. For example, an high expression of IL-1β in microglia cells surrounding Aβ plaques was observed in AD patients. Moreover, the neuroinflammation observed in neurological disorders has a pivotal role in exacerbating Aβ burden and tau hyperphosphorylation, suggesting that stimulating cytokines in response to an undesirable external response could be a checkpoint for treating neurological disorders.

The purpose of this collection is to provide the most updated research on crucial molecular pathways involved in neuroinflammation. Deciphering inflammatory biomarkers and their function in the CNS pathophisiology has important implications for understanding the pathogenesis of most of important CNS disorders.


Image credit: Design_Cells / Shutterstock

There are currently no articles in this collection.

Submission Guidelines

Back to top

This Collection welcomes submission of Research Articles. Before submitting your manuscript, please ensure you have read the submission guidelines of the journal you are submitting to, whether it's BMC Neurology or BMC Neuroscience. Articles for this Collection should be submitted via our submission system, SNAPP, on BMC Neurology or BMC Neurocience. During the submission process you will be asked whether you are submitting to a Collection, please select "Neuroinflammation and Brain Disease" from the dropdown menu.

Articles will undergo the standard peer-review process of the journal they are considered in (BMC Neurology, BMC Neuroscience) and are subject to all of the journal’s standard policies. Articles will be added to the Collection as they are published.

The Guest Editors have no competing interests with the submissions which they handle through the peer review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests.