Emerging Mechanisms in Neuroinflammation: Potential Therapeutic Targets for Neurodegenerative Diseases

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About this Research Topic

Submission deadlines

  1. Manuscript Summary Submission Deadline 31 January 2025 | Manuscript Submission Deadline 14 May 2025

  2. This Research Topic is still accepting articles.

Background

Neuroinflammation is a burgeoning area of research within the field of neurodegenerative diseases (NDs), which include Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), and Alzheimer’s disease (AD). These disorders are characterized by progressive functional loss in specific brain regions, manifesting as clinical symptoms such as memory impairment and motor dysfunction. NDs are multifactorial, with diverse etiological contributors such as abnormal protein aggregation, mitochondrial dysfunction, excitotoxicity, altered synaptic communication, cellular senescence, and impaired ion homeostasis. Recent studies have highlighted the significant role of neuroinflammation, mediated by damage-associated molecular patterns, cytokines, chemokines, and reactive oxygen species, in the pathogenesis of NDs. Despite accumulating evidence from clinical and preclinical studies validating the role of neuroinflammation, there remains a critical need to deepen our understanding of the molecular and cellular pathways involved in this process and identify potential therapeutic targets.

This Research Topic aims to elucidate the mechanisms responsible for neuroinflammation during the development of neurodegenerative diseases and identify potential therapeutic targets for future treatments. The primary objectives include answering specific questions about the molecular and cellular pathways altered during neuroinflammation and testing hypotheses related to the involvement of small molecules, cytokine signaling, and nucleoproteins in these processes. By addressing these questions, the research aims to uncover new insights that could pave the way for innovative therapeutic strategies.

To gather further insights into the boundaries of neuroinflammation in neurodegenerative diseases, we welcome articles addressing, but not limited to, the following themes:

- Small molecules, including damage-associated molecular patterns, involved in neuroinflammation (peptides, non-coding RNA, circular RNA, and others)
- Cytokine signaling influencing neuronal and glial cell communication
- Small molecules and cytokine signaling influencing synaptic integrity and function
- Nucleoproteins modulated by cytokines in neurodegenerative processes
- Cytokine signaling in abnormal protein aggregation and deposition in aging brains

In vitro and in vivo studies investigating these mechanisms are encouraged. Additionally, we invite original research articles, reviews, systematic reviews, meta-analyses, and mini-reviews covering recent progress in ND-associated neuroinflammation. Clinical case reports presenting glia-related neuroinflammatory responses using imaging or histopathological tools are specifically encouraged.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Case Report
  • Data Report
  • Editorial
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review
  • Opinion

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Keywords: Neurodegenerative diseases, Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, amyotrophic lateral sclerosis, Neuroinflammation

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