Neuroinflammation in Huntington’s Disease: Detrimental Crosstalk

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 73

Special Issue Editors


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Guest Editor
Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L'Aquila, Italy
Interests: neurodegeneration; neurodegenerative disorders; neuronal cell rearrangement; Parkinson; PPARs
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Guest Editor
Department of Life, Health and Environmental Sciences, University of L’Aquila, 67100 L'Aquila, Italy
Interests: neurodegenerative diseases; neurodegeneration; neurological disorders; Parkinson’s disease; probiotics; neuropathic pain; stem cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Huntington’s disease (HD) is a devastating condition caused by the repeat expansion of the CAG trinucleotide in exon 1 of the HTT gene, culminating in the production of a mutant huntingtin (mHtt) protein with an extended polyglutamine tract and a toxic gain-of-function. In a number of decades, efforts from researchers across the globe have led to a clear depiction of the consequences of such genetic alteration, paving the way for the development of therapeutic strategies. However, our understanding of the pathophysiology of HD is not complete. Most of all, there is a lack of knowledge as to how the mutated protein spreads across the organism, affecting different cells and tissues in different ways, particularly the brain. In the central nervous system (CNS), mHtt impairs its neuronal physiology by altering molecular systems and the surrounding microenvironment, ultimately causing neuroinflammation. In this context, the involvement of glial cells in the establishment of detrimental pro-inflammatory crosstalk with HD-affected neurons is crucial. Thus, the aim of this Special Issue is to collect studies or review articles describing such crosstalk and the journey of the mHtt protein into the CNS, demonstrating the cellular rearrangements and dynamics that are eventually involved. Moreover, studies or review articles describing the potentiality of restoring anti-inflammatory crosstalk—ultimately from a therapeutic point of view—are most welcomed.

Dr. Michele D'Angelo
Dr. Vanessa Castelli
Guest Editors

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Keywords

  • Huntington’s disease
  • mutant huntingtin (mHtt) protein
  • central nervous system
  • mutated protein
  • glial cells

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