Neural Plasticity

Stress-Induced Glial Changes in Neurological Disorders 2021


Publishing date
01 Oct 2021
Status
Open
Submission deadline
21 May 2021

Lead Editor

1Sichuan Normal University, Sichuan, China

2Shandong University, Jinan, China

3University of Manchester, Manchester, UK

4Texas A&M University, College Station, USA


Stress-Induced Glial Changes in Neurological Disorders 2021


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Description

Stress is an evolutionarily benefit to all lives, but overwhelming stress is a critical causing factor for many neurological disorders, for example, oxidative stresses are important factors in neural degenerative disorders, possibly due to increased levels of reactive oxygen species. Stress includes both physiological stress and psychological stress, and recently it is found that even psychological stress can induce mental disorders or neurological disorders. Sometimes, stress can induce very long-lasting changes in the neural circuits underlying emotional regulation, which facilitate some neurological diseases. Recent studies have shown that stress is related to changes in hippocampal function and structure, which might be mediated through increased glucocorticoids, decreased BDNF, and decreased neurogenesis. And stress finally induces behavioral, endocrine, and neural changes related, thus, to neurological disorders.

Even though many studies have suggested that stress can induce neurological disorders, but the mechanisms by which stress inducing changes are very complicated, for example, early life stress can induce emotional depression in adult life, which suggests that stress can induce some epigenetic changes or neural changes. Recently, it has been found that astrocytes can form a kind of glymphatic system, which plays an important role in clearing the extracellular dusts, such as a-beta in Alzheimer’s disease. It is postulated that stress induced failure of glymphatic clearance leads to the accumulation of neurotoxic metabolic byproducts, contributing to the suppression of cognitive function and additional neuronal loss in Alzheimer’s disease, or contributing to the affective dysfunction in major depressive disorders. Similarly, it is found that chronic stress can induce α-syn clustering, which induced impairment of dopaminergic neurons in the striatum in Parkinson’s disease. Chronic stress induced a-syn clustering is due to the impairment of the house-keeping work of glial cells. This idea is provocative, because if experimentally substantiated, it demonstrates that it may be possible to reverse the cognitive impairment of patients suffering from multi-infarct dementia. Improving glymphatic pathway function should reduce the accumulation of neurotoxic waste products, such as soluble amyloid or tau peptides, and thereby improve neuronal function. Astrocytes are the most numerous glial cells in the brain and were thought be passively providing only metabolic and physical support for neurons, serving as the primary source of energy and keep ionic homeostasis and buffering extracellular K+. Current research has expanded our knowledge and found that astrocytes can actively regulate these processes, activated by Ca2+ signaling. In addition to astrocytes, many other kinds of glial cells, such as oligodendrocytes and microglia cells, are also involved in neurological disorders.

Therefore, the aim of this Special Issue is to collect recent studies about stress induced glial changes, especially the glymphatic system, to probe the mechanisms underlying the neurological disorders, including, but not limited to Alzheimer’s disease, Parkinson’s disease, or major depressive disorders. Both original research and review articles are welcomed.

Potential topics include but are not limited to the following:

  • Early life, or traumatic, stress induced glial changes, including astrocytes and microglial changes
  • Molecular mechanisms that activate astrocytes underlying the stress induced changes
  • Functional changes of astrocytes by stress, including the buffering ability
  • Glymphatic changes in glial cells after stress
  • Epigenetic or protein expression changes in astrocytes and microglia, such as Kir4.1
  • Drugs that affect astrocytes or microglia in neurological diseases
Neural Plasticity
 Journal metrics
Acceptance rate53%
Submission to final decision58 days
Acceptance to publication37 days
CiteScore6.900
Impact Factor3.093