Special Issues

Inflammation-Mediated Responses in the Development of Neurodegenerative Diseases
Editor: Talha Bin Emran

Submission Deadline: 30 October 2024 (Status: Open)


Special Issue Editor(s)


Dr. Talha Bin Emran      Email   |   Website
1. Department of Pathology and Laboratory Medicine, Warren Alpert Medical School & Legorreta Cancer Center, Brown University, Providence, RI, USA
2. Department of Pharmacy, Faculty of Allied Health Sciences, Daffodil International University, Dhaka, Bangladesh
3. Department of Pharmacy, BGC Trust University Bangladesh, Chittagong, Bangladesh

Interests: cancer; catural croduct chemistry; immunology; phytochemistry; bioinformatics; biology


Special Issue Information

Dear Colleagues,

Neurodegenerative diseases cause central nervous system neuron degeneration. Chronic inflammation which typically accompanies these disorders worsens the illness. The degenerative evolution of these incapacitating illnesses is accelerated by continuous inflammation, which damages neuronal integrity. Neuroinflammation stimulates brain immune cells known as microglia. Damage, infection, or abnormal protein accumulations activate microglia, which creates pro-inflammatory cytokines and reactive oxygen species. These substances may cause neuronal damage and create a hazardous environment for nearby nerve cells. Astrocytes, a sort of glial cell, also can contribute to neuroinflammation. Astrocytes release pro-inflammatory molecules like interleukin-1β (IL-1 β) and TNF-α in response to neurodegenerative diseases. These substances prolong neuronal damage by promoting inflammation. Neuroinflammation may compromise the blood-brain barrier (BBB), a membrane which protects the brain from circulating blood. Inflammatory processes may weaken the BBB, allowing immune cells and inflammatory mediators to enter the brain. This influx can increase inflammation and promote neurodegeneration. Neuroinflammation depends on immune system signaling chemicals called cytokines. Many neurodegenerative diseases are linked to elevated levels of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α in the brain. These cytokines increase inflammation and neural damage.

Oxidative stress—an imbalance in reactive oxygen species (ROS) production and the organism's ability to counteract them—is linked to inflammation. Oxidative stress may damage neuronal proteins, lipids, and DNA, causing their dysfunction and potentially death. Many neurodegenerative diseases contain abnormal protein clumps, such as amyloid-beta in Alzheimer's disease and alpha-synuclein in Parkinson's disease. Protein aggregates may cause an immune response and brain inflammation. Inflammation in neurodegenerative diseases may cause a cycle. Neurodegeneration continues due to immune cell activation and pro-inflammatory mediator synthesis caused by neuronal damage.

Understanding the role of inflammation in neurodegenerative illnesses has led to treatments for immune response regulation and reduction of inflammation. This condition may be addressed by anti-inflammatory drugs, immune-modulating therapy, and lifestyle changes to improve brain function. Inflammation is present in many neurodegenerative conditions, although its causes and mechanisms vary. Thus, ongoing research aims to understand the unique properties of inflammation in each neurodegenerative condition and develop more effective treatments.

Dr. Talha Bin Emran
Guest Editor


Keywords

neurodegenerative diseases; central nervous system; chronic inflammation; immune cells; oxidative stress; immune response


Manuscript Submission Information

Manuscripts should be submitted via our online editorial system at https://www.biolifesas.org/journalx_brha/authorLogOn.action by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. Submitted manuscripts should be well formatted in good English.

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    Firdous Sayeed Mohammed, Snehasis Kundu, Vaishali R. Undale, Mayur Mali, Nahla S. Zidan, Mohamed I. Sakran, Mostafa M. Gouda
    Journal of Biological Regulators and Homeostatic Agents. 2024, 38(8): 5669-5682. https://doi.org/10.23812/j.biol.regul.homeost.agents.20243808.455
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    A variety of events, including infection, traumatic brain damage, neurodegenerative illnesses, and autoimmune disorders, can cause neuroinflammation, a complicated biological reaction in the central nervous system. Glial cells, especially microglia and astrocytes, are activated as part of this complex event, which also results in the production of pro-inflammatory cytokines, chemokines, and reactive oxygen species. In this review, the role of microglia and astrocytes in neuroinflammation, as well as the important neuroinflammatory factors including their pathways, and positive and negative aspects of neuroinflammation are discussed. It was earlier documented that microglial cells and astrocytes play a notable role in immune and inflammatory diseases. Various pro-apoptotic pathways like nuclear factor kappa B (NF-κB), cytokines, cyclooxygenases, reactive oxygen species (ROS), and mitogen-activated protein kinase (MAPK) are responsible for the induction of neuroinflammation. Neuroinflammation may also lead to many neurodegenerative diseases like Alzheimer's disease, multiple sclerosis, and Parkinson's disease. It has also been reported that inflammasomes and multi-protein oligomers are also responsible for neuroinflammation.