Emerging Role of Neuron-Glia in Neurological Disorders: At a Glance

Abstract

Based on the diverse physiological influence, the impact of glial cells has become much more evident on neurological illnesses, resulting in the origins of many diseases appearing to be more convoluted than previously happened. Since neurological disorders are often random and unknown, hence the construction of animal models is difficult to build, representing a small fraction of people with a gene mutation. As a result, an immediate necessity is grown to work within in vitro techniques for examining these illnesses. As the scientific community recognizes cell-autonomous contributions to a variety of central nervous system illnesses, therapeutic techniques involving stem cells for treating neurological diseases are gaining traction. The use of stem cells derived from a variety of sources is increasingly being used to replace both neuronal and glial tissue. The brain’s energy demands necessitate the reliance of neurons on glial cells in order for it to function properly. Furthermore, glial cells have diverse functions in terms of regulating their own metabolic activities, as well as collaborating with neurons via secreted signaling or guidance molecules, forming a complex network of neuron-glial connections in health and sickness. Emerging data reveals that metabolic changes in glial cells can cause morphological and functional changes in conjunction with neuronal dysfunction under disease situations, highlighting the importance of neuron-glia interactions in the pathophysiology of neurological illnesses. In this context, it is required to improve our understanding of disease mechanisms and create potential novel therapeutics. According to research, synaptic malfunction is one of the features of various mental diseases, and glial cells are acting as key ingredients not only in synapse formation, growth, and plasticity but also in neuroinflammation and synaptic homeostasis which creates critical physiological capacity in the focused sensory system. The goal of this review article is to elaborate state-of-the-art information on a few glial cell types situated in the central nervous system (CNS) and highlight their role in the onset and progression of neurological disorders.

The potential therapeutic roles of Rho GTPases in substance dependence

“…Although the current neurobiological mechanism of opioid abuse is primarily related to synaptic plasticity of dopaminergic and glutaminergic neurons, this drug-induced plasticity may also be enhanced by glial cell activity. More and more evidence showed that glial cells, including oligodendrocytes, astrocytes and microglia, participate in cognitive impairment-and drug-induced neuronal plasticity changes, through the activity of cytokines and neurotrophins ( Rahman et al, 2022 ). Chronic morphine therapy induces activation of astrocytes and microglia ( Valentinova et al, 2019 ).…”

Review on the neuron damage parameters in patients with end-stage renal disease

“…This process is called demyelination. Messages that pass along a demyelinated nerve become delayed or blocked [19].…”

Drosophila Bchsoverexpression recapitulates humanWDFY3neurodevelopmental phenotypes with implications for glial cell involvement in altered head circumference

“…2020; Lago-Baldaia et al . 2020; Rahman et al . 2022), they have received rather little attention in the effort to unravel WDFY3 -associated pathomechanisms.…”

“…Currently an increasing number of studies concentrate on loss of WDFY3/Bchs and its effects on the nervous system with a focus on neuronal impairment. Although glial cells are known to play an essential role for neuronal function and neurodevelopment (Bittern et al 2021;Kim et al 2020;Lago-Baldaia et al 2020;Rahman et al 2022), they have received rather little attention in the effort to unravel WDFY3-associated pathomechanisms. So far, it was shown that loss of Wdfy3 is accompanied with mislocalisation of glial guidepost cells, which provide guidance cues for the formation of axonal tracts (Dragich et al 2016).…”