Contents
Special Issue Topic

Neuroinflammation in the Ageing and the Injured Brain

Submission Deadline: June 30, 2025

Guest Editors

Prof. Ameneh Rezayof E-Mail

Professor at the Department of Animal Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran

Research Keywords: Neurobiology of memory formation, reward-related learning in drug addiction, and signaling pathways in emotional behaviours

Dr. Maryam Sardari E-Mail

Assistant Professor at the Department of Animal Biology, School of Biology, College of Science, University of Tehran, Tehran, Iran

Research Keywords: Stroke, neuroinflammation, glial activation, peripheral immune system, behavioral neuroscience

About the Special lssue

Immune system dysregulation is a significant consequence of aging. Pathological changes in central and peripheral immune responses trigger neuronal injury in humans and laboratory animals. Neuroinflammation can occur via activating microglial cells and other immune cells to increase the release of cytokines, reactive oxygen and nitrogen species, prostaglandins and growth factors in the aging brain. Age-related neuroinflammation is a central mechanism in Alzheimer's disease (AD), Parkinson's disease (PD), and other neurodegenerative disorders commonly characterized by cognitive impairment, dementia, and disability. The sustained brain's immune activation may be correlated with the presence of amyloid β plaques and neurofibrillary tangles in AD pathogenesis. Microglia-derived oxidative stress plays a critical role in severe neuroinflammation and α-synuclein pathogenic alteration to induce progressive dopaminergic nigrostriatal degeneration associated with motor dysfunction in PD. Moreover, neuroinflammation and oxidative stress contribute to the dysregulation of cerebral blood flow and the breakdown of blood brain barrier implicated in the pathogenesis of age-associated neurodegenerative disorders.

Neuroinflammation in the ageing and the injured brain is a special issue that focuses on the inflammatory mechanisms involved in age-related neurodegenerative diseases. This issue brings together work focusing on the critical role of central and peripheral neuro-immune interactions. Clinical and sub-clinical studies for integrative reviews and commentaries on brain neuroinflammation and neurodegeneration are encouraged and welcome.

Keywords: Aging, neuroinflammation, neurodegenerative diseases

Published Articles

Open Access Review
Functional interactions between neurotransmitters and neuropeptides in regulating suprachiasmatic nucleus function and circadian rhythms
The overt expression of circadian rhythms is a manifestation of the suprachiasmatic nucleus (SCN). This integrated complex function based on the transcriptional/translational feedback loops (TFFLs),
Published: September 24, 2024 Explor Neurosci. 2024;3:434–477
2801 62 0
Open Access Perspective
Mesenchymal stem cell stroke therapy: current limitations in its clinical translation
For more than a decade now, research studies, proof of concept work, and clinical trials have endeavored to understand how mesenchymal stem cells might be used to help protect, repair, and/or regene
Published: June 28, 2023 Explor Neurosci. 2023;2:98–105
2640 53 1
Open Access Review
Cellular and molecular mechanisms of stress-induced memory impairment
Exposure to stressful conditions plays a critical role in brain processes, including neural plasticity, synaptic transmission, and cognitive functions. Since memory-related brain regions, the hippocampus (Hip), the amygdala, and the prefrontal cortex, express high glucocorticoid receptors (GRs), these areas are the potential targets of stress hormones. Stress affects memory encoding, consolidation, and retrieval, which may depend on many factors such as the type, duration, the intensity of the stressor or the brain region. Here, this review mainly focused on the mechanisms involved in stress-induced memory impairment. Acute/chronic stress induces structural and functional changes in neurons and glial cells. Dendritic arborization, reduction of dendritic spine density, and alteration in glutamatergic-mediated synaptic transmission via N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors are mechanisms that stress affect long-term memory formation. Exposure to acute or chronic stress could interplay with multiple neurotransmitter signaling, modulating the neuronal circuits involved in memory impairment or state-dependent learning. Stress hormones also modulate the expression of microRNAs in the specific brain regions responsible for stress-induced behaviors. Because of expressing GRs in astrocytes and microglial cells, stress could affect the morphology, structure, and functions of these glial cells in memory-related brain regions. Astrocytes play a crucial role in stress-induced aversive or fear memory formation. Over-activation of the microglial cells enhances the release of inflammatory cytokines, which results in neuronal injury. Stress has a prominent role in cognitive decline to induces memory problems, particularly in older adults. Due to the issue’s importance, here the provided overview attempted to address the question of how stress alters neuronal epigenetic regulators, synaptic transmissions, and glial activity in the brain.
Published: December 30, 2022 Explor Neurosci. 2022;1:100–119
6368 120 1
Completed Special Issues