Neuroinflammation refers to the inflammatory response within the central nervous system (CNS), a complex process that involves the activation of glial cells, the release of proinflammatory cytokines, and changes in brain physiology. These responses are intended to protect the brain from harmful stimuli, such as pathogens or injury. However, chronic neuroinflammation has been implicated in various neurodegenerative diseases, including Alzheimer's, Parkinson's, and multiple sclerosis, highlighting the dual role of inflammation as both protective and detrimental.

Microglia, the resident immune cells of the CNS, play a pivotal role in mediating neuroinflammatory responses. Under normal circumstances, microglia contribute to homeostasis by monitoring the brain's environment, clearing debris, and supporting neuronal health. However, upon activation due to injury or disease, these cells change their morphology, proliferate, and release a range of proinflammatory markers, including cytokines (such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6)), chemokines, and reactive oxygen species (ROS). This activation can lead to a cascade of events, affecting neuronal function, integrity, and survival.

The distribution of proinflammatory markers in the brain varies by region and context. For instance, in Alzheimer's disease, research has shown that areas such as the hippocampus and cortex exhibit elevated levels of proinflammatory cytokines and marked microglial activation. Studies have demonstrated that the accumulation of amyloid-beta plaques, a hallmark of Alzheimer’s pathology, is associated with increased expression of cytokines like IL-1β and TNF-α, suggesting that neuroinflammation could both result from and contribute to amyloid pathology. The distribution of these markers often correlates with the severity of cognitive decline, underscoring the importance of controlling neuroinflammation for potential therapeutic strategies.

Further complicating the picture, the blood-brain barrier (BBB) plays a crucial role in regulating the entry of circulating immune cells and their inflammatory mediators into the CNS. In conditions of neuroinflammation, the integrity of the BBB can be compromised, allowing for greater infiltration of proinflammatory cells and factors. This breach may lead to exacerbated inflammation, creating a vicious cycle that amplifies neurodegenerative processes.

Various imaging techniques, including positron emission tomography (PET), have provided insights into the dynamics and distribution of neuroinflammatory markers in vivo. These advancements allow researchers to visualize and quantify the brain’s inflammatory response across different neurodegenerative conditions, facilitating a better understanding of disease progression and potential therapeutic interventions.

In conclusion, neuroinflammation serves as a double-edged sword in the brain, with proinflammatory markers demonstrating varied distributions that are context-dependent. The role of microglia, the involvement of specific cytokines, and the effects of BBB integrity all contribute to the complex landscape of neuroinflammatory responses. A deeper understanding of these mechanisms is crucial for developing targeted therapies that could mitigate the harmful effects of chronic inflammation in neurodegenerative diseases, offering hope for improved outcomes for affected individuals.

It is the goal of this research theme to collect original research, reviews, and meta-analyses to demonstrate the role of neuroinflammation in the pathogenesis and developing therapeutics for diverse neurological diseases. The scope will cover the following aspects, but is not limited to them:

•Clinical studies demonstrating the therapeutic efficacy of novel treatments in managing neuroinflammatory diseases.

•Basic original research on the underlying mechanisms of neurological diseases involving neuroinflammation or distribution of inflammatory markers in the central nervous system, like detailed anatomical mapping.

•Systemic reviews of or meta-analysis on the therapeutics including traditional or complementary medicine or individual bioactive compounds on the above conditions and their underlying mechanisms.

We encourage the submission of both in vitro and in vivo studies that will make a significant contribution to the revelation of underlying mechanisms of herbal recipes, individual bioactive compounds, or a combination of a few of them. These studies will pave the way to discovering new effective therapeutics to treat neurological disorders.

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Frontiers in Aging Neuroscience

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