Background:
The pathophysiology of Huntington's disease (HD), a neurodegenerative condition, is considered to also involve glial cells. Understanding the intricate interactions between neurons and glia can be accomplished by looking at gliogenic pathways and transcriptional dysregulation. Understanding glial involvement may result in novel medicines, biomarkers, and a thorough understanding of HD's molecular foundation, thereby altering patient outcomes and disease management.
Methods:
Databases including PubMed, MEDLINE and Google Scholar were searched for published articles without any date restrictions, involving Huntington’s disease, gliogenesis, gliogenic genes and signaling pathways, astrocytogenic genes.
Results:
This study reveals the complex interactions between gliogenic pathways and disease etiology. Key factors Pax6, Nkx6.1, Sox9, Sox4, and NFIX are impacted by transcriptional dysregulation, which may interfere with gliogenesis and cellular differentiation. TGF-beta, JAK-STAT, SHH, and NF-B dysregulated signaling pathways emphasize their part in astrocyte dysfunction and glial-neuronal interactions. GFAP, S100, and NF-B are implicated in neuroprotection and are also involved in HD pathogenesis. The intricate interplay of transcriptional factors and pathways complicates the mechanisms behind HD. Therapeutically, gliogenic pathway modulation, transcriptional balance restoration, and glial dysfunction targeting offer promising approaches to slow the course of HD. Even if there are still gaps, current research will improve our knowledge of gliogenic processes and of their possible implications in HD neurodegeneration.
Conclusion:
The investigation of gliogenic pathways and molecules in Huntington's disease (HD) reveals insights into potential glial dysfunction contributions. Alterations to signaling pathways (TGF-beta, JAK-STAT, SHH), astrocyte-related molecules (GFAP, S100, NF-B), and transcriptional dysregulation may all have an impact on how the disease develops. Complexity is added by transcription factors that affect cellular differentiation (HOPX, Sox9, Sox4, NFIX). The interaction between pathways emphasizes how complex HD pathogenesis is. Genetic and epigenetic alterations, stress reactions, and interactions between pathways all contribute to dysregulation. A growing understanding of gliogenesis and its possible implications in HD are provided in this study, opening up possibilities for therapeutic investigation and mitigating the effects of glial-driven HD.
