Damage or death of the neuron, glia, and microglia fall mainly under the umbrella of major neurological diseases including neuroinflammatory disorders, dementia, Alzheimer’s and Parkinson’s diseases, as well as viral infections such as HIV, HSV and coronavirus. Brain inflammation plays a dual role. It is neuroprotective in the acute phase response, but in the chronic condition, the activated microglia response releases a variety of proinflammatory products, such as interleukin 1 (IL-1) and IL-1β, exacerbating Aβ burden and causing tau hyperphosphorylation, a hallmark of Central Nervous System (CNS) pathophysiology. In addition viral infections, such as HSV-1, facilitate the processes of proinflammatory cytokine secretion in response to toll-like receptors (TLRs) favouring the abnormal processing of amyloid precursor protein (APP), leading to Aβ production and hyperphosphorylation of tau. Thus, neuroinflammation observed in neurological disorders has a pivotal role in exacerbating Aβ burden and tau hyperphosphorylation, suggesting that the stimulation of cytokines in response to an undesirable external response could be a checkpoint for the treatment of neurological disorders.

The positive correlation of neuroinflammation and neurological disorders documented in the literature is well established. However, it needs to be further investigated to better clarify the mechanisms of cytokine release in response to a variety of stimuli, which could be the central point for the treatment of neurological infections. Indeed, very little is known regarding the effects of neuroinflammatory mediators on Aβ production and its metabolism, mTOR activation, and hyperphosphorylation of tau. Moreover, these proinflammatory cytokines also help our immune system through a neuroprotective mechanism in clearing viral infection through recruitment of mononuclear cells, but in another instance, can also lead to CNS dysfunction and neurodegenerative syndromes. Thus, this Special Issue aims to reflect the role of cytokines as an immunological function and their synergistic effects on the mechanism of amyloid pathology and its associated factors on the development of neurodegenerative processes. A complete understanding of the role of cytokines through multidisciplinary approaches is necessary to develop an effective therapy against neurological infections

The aim of this Special Issue is to collate original articles with a focus on the roles of different types of cytokines with respect to amyloid pathology in response to different neurological disorders and viral infections. These studies may lead to the identification of new therapeutic approaches to ameliorate the dysfunction of neuroinflammation as a checkpoint to extend the survival of affected individuals. Review articles discussing the current state of the art are also welcome.

Potential topics include but are not limited to the following:

• Role of different types of viral infections in cytokines storm and amyloid pathology
• Relationship between inflammatory cytokines and Aβ production, hyper- phosphorylation of Tau and mTOR activation in neurodegeneration and ageing
• Neuroinflammation, neurodegeneration, and therapeutic approaches by targeting inflammatory mediator pathways in neurodegeneration
• Role of inflammatory response cytokines on misfolded protein intermediates/aggregation of Aβ in relation to neurodegenerative diseases
• Bioinformatics approaches such as NGS data analysis, drug discovery, artificial intelligence; deep learning and deep neural networks, and convolution neural networks to better understand the role of cytokines and the underlying molecular mechanisms of neurological disorders