Molecular and Metabolic Insights into Neuroinflammation and Neurodegeneration
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 30 November 2024 | Viewed by 2001
Special Issue Editors
Interests: neuroinflammation; neurodegeneration; inflammation; oncology; brain tumor
Special Issues, Collections and Topics in MDPI journals
Interests: molecular biology; neuroinflammation; pharmacology; inflammation; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Inflammation in central nervous system (CNS) is recognized as laying a crucial role in the pathogenesis of several neurodegenerative disorders, such as Parkinson’s (PD), Alzheimer’s (AD), and Huntington’s (HD) diseases, frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS), in addition to acute or chronic neuroinflammatory diseases, such as spinal cord injury (SCI) and traumatic brain injury (TBI). Neuroinflammation may indeed be triggered by various stimuli, like infections, the release of toxic metabolites and abnormal accumulation of proteins, and it is mediated by the cytokines, chemokines, and reactive oxygen species (ROS) released by both resident and peripheral cells. Microglia are involved in immune surveillance in the CNS and, when activated, may counteract injuries with a brief and controlled inflammatory response. However, their dysfunctional activation may lead to uncontrolled inflammation, with the continuous release of pro-inflammatory mediators and even recruitment of peripheral immune cells. Microglia senescence may also affect the progression of neurodegeneration. While reactive microglia may provide both pro- and anti-inflammatory functions, senescent dystrophic microglia are characterized by reduced motility and phagocytosis, increased ROS production, and a pro-inflammatory state; additionally, they display the potential for a significant impact on neuron viability. Furthermore, metabolic and energetic disturbances have recently been determined to be both a consequence and a cause of neurodegeneration. Despite the fact that the causes of these diseases can be polyetiological, they have a wide range of similar molecular and cellular pathophysiological processes, namely protein aggregation, glutamate toxicity, calcium, proteolytic and oxidative stress, neuroinflammation, mitochondrial dysfunction, and others associated with aging.
This Special Issue aims to highlight the numerous metabolic changes in neurodegenerative diseases and related current therapeutic approaches and to provide a more comprehensive overview of the role of neuroinflammation in the development of neurological and neurodegenerative diseases. Contributions from all research areas are welcome, including disease modeling; human neuropathology; biochemical, molecular, and clinical studies; genomics; proteomics, and therapeutic interventions.
Dr. Giovanna Casili
Dr. Marika Lanza
Guest Editors
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Keywords
- Parkinson’s disease
- Alzheimer’s disease
- metabolism
- inflammation
- neurodegeneration
- drug discovery
- pharmacological therapy
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