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May 7, 2026Journal of Biochemical and Molecular Toxicology0 citations

Novel Cellular Signalling Axes in Neurodegenerative Diseases: From NLRP3 Inflammasome to Wnt/β‐Catenin and Hippo‐YAP Pathways

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KSKuldeep SinghIAIftakhar AhmadDJDivya Jain

Key Points

  • This review aims to explore novel cellular signalling axes involved in neurodegenerative diseases.
  • Reviewed key signalling pathways associated with neurodegenerative diseases
  • Focus on NLRP3 inflammasome, Wnt/β‐catenin, and Hippo‐YAP pathways
  • Discussed implications for disease-modifying treatments
  • Identified dysregulation of key pathways in neurodegenerative diseases
  • Highlighted the role of neuroinflammation in neuronal damage
  • Demonstrated potential neuroprotective functions of these pathways

Abstract

ABSTRACT Neurodegenerative diseases (NDs), including Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), are characterised by impaired cellular homeostasis and progressive neuronal loss. Emerging evidence highlights the critical role of cellular signalling pathways in the progression and pathogenesis of these disorders. With a focus on the NLRP3 inflammasome, Wnt/β‐catenin, and Hippo‐YAP cascades, this review focuses on new signalling pathways linked to neurodegenerative disorders. Among them, the NLRP3 inflammasome is a crucial mediator of neuroinflammation, causing neuronal damage and persistent immune activation. In contrast, these pathways regulate neurogenesis, synaptic plasticity, and cell survival, offering potential neuroprotective functions. Dysregulation of these pathways disrupts cellular integrity, exacerbates disease progression, and represents a convergence point for therapeutic intervention. In NDs, knowing how these pathways interact offers fresh perspectives on disease processes and finds new targets for the creation of disease‐modifying treatments.

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Cite This Study

Singh et al. (2026) studied this question.

synapsesocial.com/papers/69fbef86164b5133a91a3752https://doi.org/10.1002/jbt.70880
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