Submission Deadline: 30 October 2024 (Status: Open)
Special Issue Editor(s)
Dr. Talha Bin Emran
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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
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